Volume 138  ·   Issue 01  ·  2025

Interstitial lung disease (ILD) encompasses diverse conditions, including fibrotic lung diseases characterized by cellular proliferation, interstitial inflammation, and fibrosis. ILD can arise from numerous causes, including connective tissue diseases (CTDs) such as systemic sclerosis (SSc), rheumatoid arthritis (RA), idiopathic inflammatory myopathy (IIM), Sjögren’s syndrome (SS), and systemic lupus erythematosus (SLE), with SSc, RA, and IIM being more prevalent. The reported prevalence of ILD varies widely across studies owing to differences in inclusion criteria, research methodologies, and follow-up durations. For instance, the prevalence of ILD in SSc can reach 30%, with a 10-year mortality rate of up to 40%.^[1]The exact prevalence of rheumatoid arthritis-associated interstitial lung disease (RA-ILD) remains uncertain, ranging from 1% to 58% based on different study methodologies.^[2]The global prevalence of ILD in polymyositis and dermatomyositis (PM/DM) is approximately 41%, with a higher prevalence in Asian populations.^[3]ILD profoundly affects the treatment approaches, quality of life, morbidity, and mortality in patients with rheumatic diseases. The overlapping pathological and clinical features of ILDs complicate diagnosis and pose significant challenges in the management of CTD-ILDs.

Neurological diseases are a major health concern, and brain injury is a typical pathological process in various neurological disorders. Different biomarkers in the blood or the cerebrospinal fluid are associated with specific physiological and pathological processes. They are vital in identifying, diagnosing, and treating brain injuries. In this review, we described biomarkers for neuronal cell body injury (neuron-specific enolase, ubiquitin C-terminal hydrolase-L1, αII-spectrin), axonal injury (neurofilament proteins, tau), astrocyte injury (S100β, glial fibrillary acidic protein), demyelination (myelin basic protein), autoantibodies, and other emerging biomarkers (extracellular vesicles, microRNAs). We aimed to summarize the applications of these biomarkers and their related interests and limits in the diagnosis and prognosis for neurological diseases, including traumatic brain injury, status epilepticus, stroke, Alzheimer’s disease, and infection. In addition, a reasonable outlook for brain injury biomarkers as ideal detection tools for neurological diseases is presented.

Gliomas are the most common primary neuroepithelial tumors of the central nervous system in adults, of which glioblastoma is the deadliest subtype. Apart from the intrinsically indestructible characteristics of glioma (stem) cells, accumulating evidence suggests that the tumor microenvironment also plays a vital role in the refractoriness of glioblastoma. The primary functions of platelets are to stop bleeding and regulate thrombosis under physiological conditions. Furthermore, platelets are also active elements that participate in a variety of processes of tumor development, including tumor growth, invasion, and chemoresistance. Glioma cells recruit and activate resting platelets to become tumor-educated platelets (TEPs), which in turn can promote the proliferation, invasion, stemness, and chemoresistance of glioma cells. TEPs can be used to obtain genetic information about gliomas, which is helpful for early diagnosis and monitoring of therapeutic effects. Platelet membranes are intriguing biomimetic materials for developing efficacious drug carriers to enhance antiglioma activity. Herein, we review the recent research referring to the contribution of platelets to the malignant characteristics of gliomas and focusing on the molecular mechanisms mediating the interaction between TEPs and glioma (stem) cells, as well as present the challenges and opportunities in targeting platelets for glioma therapy.

Oxidative stress due to aberrant metabolism is considered as a crucial contributor to diabetes and its complications. Hyperglycemia and hyperlipemia boost excessive reactive oxygen species generation by elevated mitochondrial respiration, increased nicotinamide adenine dinucleotide phosphate oxidase activity, and enhanced pro-oxidative processes, including protein kinase C pathways, hexosamine, polyol, and advanced glycation endproducts, which exacerbate oxidative stress. Oxidative stress plays a significant role in the onset of diabetes and its associated complications by impairing insulin production, increasing insulin resistance, maintaining hyperglycemic memory, and inducing systemic inflammation. A more profound comprehension of the molecular processes that link oxidative stress to diabetes is crucial to new preventive and therapeutic strategies. Therefore, this review discusses the mechanisms underlying how oxidative stress contributes to diabetes mellitus and its complications. We also summarize the current approaches for prevention and treatment by targeting the oxidative stress pathways in diabetes.

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have emerged as a revolutionary class of antidiabetic agents with demonstrated benefits extending beyond glycemic control. Dedicated renal outcome trials of SGLT2i have shown impressive renal protective effects, regardless of diabetes status.^[1,2,3]

Huaier granule is an important medicinal fungus extract widely used in cancer treatment. Previous retrospective studies have reported its effectiveness in breast cancer patients, but the imbalanced baseline characteristics of participants could have biased the results. Therefore, this retrospective study aimed to examine the efficacy of Huaier granule on the prognosis of breast cancer patients.

In this single-center cohort study, breast cancer patients diagnosed and treated at the Guangdong Provincial Hospital of Chinese Medicine between 2009 and 2017 were selected. The data were retrospectively analyzed and divided into two groups according to whether the patients received Huaier granules. The propensity score matching (PSM) method was used to eliminate selection bias. The disease-free survival (DFS) and overall survival (OS) for these groups were compared using the Kaplan–Meier method and the Cox regression.

This study included 214 early invasive breast cancer patients, 107 in the Huaier group and 107 in the control group. In the Kaplan–Meier analysis, the 2-year and 5-year DFS rates were significantly different in the Huaier group and control group (hazard ratio [HR], 0.495; 95% confidence interval [CI], 0.257–0.953; P = 0.023). The 2-year and 5-year OS rates were also significantly different (HR, 0.308; 95% CI, 0.148–0.644; P = 0.001). On multivariable Cox regression, Huaier granule was associated with improved DFS (HR, 0.440; 95% CI, 0.223–0.868; P = 0.018) and OS (HR, 0.236; 95% CI, 0.103–0.540; P = 0.001).

In this retrospective study, Huaier granules improved the DFS and OS of early invasive breast cancer patients, providing real-world evidence for further prospective studies on treating breast cancer with Huaier granules.

Knee osteoarthritis (OA) is still challenging to prevent or treat. Enhanced endoplasmic reticulum (ER) stress and increased pyroptosis in chondrocytes may be responsible for cartilage degeneration. This study aims to investigate the effect of ER stress on chondrocyte pyroptosis and the upstream regulatory mechanisms, which have rarely been reported.

The expression of the histone methyltransferase enhancer of zeste homolog 2 (EZH2), microRNA-142-3p (miR-142-3p), and high mobility group box 1 (HMGB1) and the levels of ER stress, pyroptosis, and metabolic markers in normal and OA chondrocytes were investigated by western blotting, quantitative polymerase chain reaction, immunohistochemistry, fluorescence in situ hybridization, fluorescein amidite-tyrosine-valine-alanine-aspartic acid-fluoromethyl ketone (FAM-YVAD-FMK)/Hoechst 33342/propidium iodide (PI) staining, lactate dehydrogenase (LDH) release assays, and cell viability assessments. The effects of EZH2, miR-142-3p, and HMGB1 on ER stress and pyroptosis and the hierarchical regulatory relationship between them were analyzed by chromatin immunoprecipitation, luciferase reporters, gain/loss-of-function assays, and rescue assays in interleukin (IL)-1β-induced OA chondrocytes. The mechanistic contribution of EZH2, miR-142-3p, and HMGB1 to chondrocyte ER stress and pyroptosis and therapeutic prospects were validated radiologically, histologically, and immunohistochemically in surgically induced OA rats.

Increased EZH2 and HMGB1, decreased miR-142-3p, enhanced ER stress, and activated pyroptosis in chondrocytes were associated with OA occurrence and progression. EZH2 and HMGB1 exacerbated and miR-142-3p alleviated ER stress and pyroptosis in OA chondrocytes. EZH2 transcriptionally silenced miR-142-3p via H3K27 trimethylation, and miR-142-3p posttranscriptionally silenced HMGB1 by targeting the 3′-UTR of the HMGB1 gene. Moreover, ER stress mediated the effects of EZH2, miR-142-3p, and HMGB1 on chondrocyte pyroptosis. In vivo experiments mechanistically validated the hierarchical regulatory relationship between EZH2, miR-142-3p, and HMGB1 and their effects on chondrocyte ER stress and pyroptosis.

A novel EZH2/miR-142-3p/HMGB1 axis mediates chondrocyte pyroptosis and cartilage degeneration by regulating ER stress in OA, contributing novel mechanistic insights into OA pathogenesis and providing potential targets for future therapeutic research.

Renal osteodystrophy (ROD) is a skeletal pathology associated with chronic kidney disease-mineral and bone disorder (CKD-MBD) that is characterized by aberrant bone mineralization and remodeling. ROD increases the risk of fracture and mortality in CKD patients. The underlying mechanisms of ROD remain elusive, partially due to the absence of an appropriate animal model. To address this gap, we established a stable mouse model of ROD using an optimized adenine-enriched diet and conducted exploratory analyses through ribonucleic acid sequencing (RNA-seq).

Eight-week-old male C57BL/6J mice were randomly allocated into three groups: control group (n = 5), adenine and high-phosphate (HP) diet group (n = 20), and the optimized adenine-containing diet group (n = 20) for 12 weeks. We assessed the skeletal characteristics of model mice through blood biochemistry, microcomputed tomography (micro-CT), and bone histomorphometry. RNA-seq was utilized to profile gene expression changes of ROD. We elucidated the functions of differentially expressed genes (DEGs) using gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and gene set enrichment analysis (GSEA). DEGs were validated via quantitative real-time polymerase chain reaction (qRT-PCR).

By the fifth week, adenine followed by an HP diet induced rapid weight loss and high mortality rates in the mouse group, precluding further model development. Mice with optimized adenine diet-induced ROD displayed significant abnormalities in serum creatinine and blood urea nitrogen levels, accompanied by pronounced hyperparathyroidism and hyperphosphatemia. The femur bone mineral density (BMD) of the model mice was lower than that of control mice, with substantial bone loss and cortical porosity. ROD mice exhibited substantial bone turnover with an increase in osteoblast and osteoclast markers. Transcriptomic profiling revealed 1907 genes with upregulated expression and 723 genes with downregulated expression in the femurs of ROD mice relative to those of control mice. Pathway analyses indicated significant enrichment of upregulated genes in the sphingolipid metabolism pathway. The significant upregulation of alkaline ceramidase 1 (Acer1), alkaline ceramidase 2 (Acer2), prosaposin-like 1 (Psapl1), adenosine A1 receptor (Adora1), and sphingosine-1-phosphate receptor 5 (S1pr5) were successfully validated in mouse femurs by qRT-PCR.

Optimized adenine diet mouse model may be a valuable proxy for studying ROD. RNA-seq analysis revealed that the sphingolipid metabolism pathway is likely a key player in ROD pathogenesis, thereby providing new avenues for therapeutic intervention.

Leukocyte telomere length (LTL) shortening, a biomarker of telomere attrition, has been linked to multiple diseases. However, the relationship between LTL and digestive diseases remains uncertain. This study aimed to investigate the association between LTL and the risk of digestive diseases.

A cohort analysis of over 500,000 participants from the UK Biobank (UKB) between 2006 and 2021 was conducted to estimate the associations of LTL with more than 90 common digestive diseases. LTL was quantified using multiplex quantitative polymerase chain reaction, and cases of each disease were determined according to inpatient and primary care data. Multivariable Cox proportional hazards regression analysis was used to evaluate the associations of LTL with the risk of digestive diseases. Furthermore, such associations were also evaluated after stratification by sex and ethnicity.

After a mean follow-up time of 11.8 years, over 20 International Classification of Diseases, 10th Revision (ICD-10) codes were showed to be associated with telomere attrition. LTL shortening is associated with an increased risk of several digestive diseases, including gastroesophageal reflux disease (K21: hazard ratio [HR] = 1.30, 95% confidence interval [95% CI]: 1.19–1.42), esophageal ulcer (K221: HR = 1.81, 95% CI: 1.22–2.71), Barrett’s esophagus (K227: HR = 1.58, 95% CI: 1.14–2.17), gastritis (K29: HR = 1.39, 95% CI: 1.26–1.52), duodenal ulcer (K26: HR = 1.55, 95% CI: 1.14–2.12), functional dyspepsia (K30X: HR = 1.36, 95% CI: 1.06–1.69), non-alcoholic fatty liver disease (NAFLD) (K760: HR = 1.39, 95% CI: 1.09–1.78), liver cirrhosis (K74: HR = 4.73, 95% CI: 3.27–6.85), cholangitis (K830: HR = 2.55, 95% CI: 1.30–5.00), and hernia (K43: HR = 1.50, 95% CI: 1.17–1.94; K44: HR = 1.29, 95% CI: 1.17–1.42). The risk of rectal polyps (K621: HR = 0.77, 95% CI: 0.63–0.92) decreased per unit shortening of LTL.

This study suggests that LTL shortening is associated with an increased risk of most digestive diseases except for rectal polyps. These findings may provide some clues for understanding the pathogenesis of digestive diseases.

As an essential part of health services, rehabilitation is of great significance to improve the health and quality of life of the whole population. Accelerating aging calls for a significant expansion of rehabilitation services in China, but rehabilitation needs remain unclear. We conducted the study to explore the rehabilitation needs in China and project the trend of rehabilitation needs from 2020 to 2034.

The data of health conditions that might potentially benefit from rehabilitation were obtained from Global Burden of Disease (GBD) study. Estimated annual percentage changes (EAPCs) were calculated to quantify the trends of the age-standardized rates. Projections of rehabilitation needs were made until 2034 using Bayesian age–period–cohort analysis (BAPC).

Approximately 460 million persons (33.3% of the total population) need rehabilitation in China, contributing to 63 million years lived with disabilities (YLDs) in 2019. The number of prevalent cases that need rehabilitation increased from around 268 (95% uncertainty interval [UI]: 257–282) million in 1990 to almost 460 (95% UI: 443–479) million in 2019, representing an increase of 71.3%. The highest contribution to the need for rehabilitation was musculoskeletal disorders with about 322 (95% UI: 302–343) million persons in seven aggregate disease and injury categories, and hearing loss with over 95 (95% UI: 84–107) million people among 25 health conditions. Based on the projection results, there will be almost 636 million people (45% of the total population) needing rehabilitation services in China by 2034, representing an increase of 38.3%. The rehabilitation needs of neoplasms, cardiovascular diseases, and neurological disorders are expected to increase significantly from 2019 to 2034, with increases of 102.3%, 88.8% and 73.2%, respectively.

The need for rehabilitation in China substantially increased over the last 30 years. It is predicted that over two in five people will require rehabilitation by 2034, thus suggesting the need to develop rehabilitation services that meet individuals’ rehabilitation needs.

Without timely and effective rehabilitation, hearing loss may profoundly affect human life quality. China has a large population of hearing-impaired individuals, which imposes a heavy health burden on society. Moreover, this population is projected to increase rapidly owing to China’s aging society.

We used data from a population-representative epidemiological investigation of hearing loss and ear diseases in four Chinese provinces. We estimated the national prevalence using multiple linear regression of the age-group proportions and prevalence in 31 provinces with clustering analysis. We used years lived with disability (YLDs) to analyze the disease burden and forecasted the prevalence of hearing loss by 2060 in China.

An estimated 115 million people had moderate-to-complete hearing loss in 2015 across the 31 provinces of China (8.4% of 1.37 billion people). Of these, 85.7% were older than age 50 years (99 million people) and 2.4% were younger than 20 years old (2.8 million people). Of all YLDs attributable to hearing loss, 68.9% were attributable to moderate-to-complete cases. By 2060, a projected 242 million people in China will have moderate-to-complete hearing loss, a 110.0% increase from 2015.

The hearing loss prevalence in China is high. Population aging and socioeconomic factors substantially affect the prevalence and severity of hearing loss and the disease burden. The prevalence and severity of hearing loss are unevenly distributed across different provinces. Future public health policies should take these trends and regional variations into account.

Ulcerative colitis (UC) and Crohn’s disease (CD) are chronic inflammatory bowel diseases (IBDs) with largely unclear etiologies and complex pathogeneses. The pathogenesis of UC has been linked to an imbalance in the gut microbiota, including in the prevalence of Enterobacteriaceae, especially pathogenicEscherichia coli(E. coli).^[1]The UC diagnosis and assessment primarily rely on colonoscopy and mucosal biopsy pathology, which are limited by their invasiveness, constraints on medical resources, and potential risks and complications. Several biomarkers, such as serum C-reactive protein (CRP), fecal calprotectin, and fecal lactoferrin, are currently recommended for assessing UC disease activity. However, these markers are primarily inflammation-related factors produced by the host, not specific to IBD, and are influenced by other inflammatory states. Microbiome-related biomarkers are used as direct indicators of the gut microecosystem and have considerable potential for disease assessment and therapeutic guidance in IBD. However, current analyses of gut microbiota, such as 16S rRNA or metagenomic sequencing, are often time-consuming and costly. Siderophore, a low-molecular-weight protein secreted extracellularly to chelate ferric iron, is a crucial virulence factor in iron acquisition of bacteria and fungi. The presence of siderophores can indirectly reflect bacterial abundance and activity.^[2]Gram-negative pathogens (E. coli,Klebsiella,Shigella,Salmonella, andYersinia) have four common types of siderophores, including enterobactin, salmochelin, aerobactin, and yersiniabactin.^[3]Here, we aimed to explore the relationships between positivity rates and copy numbers of siderophore genes and clinical characteristics of UC to evaluate their potential as noninvasive biomarkers for assessing UC disease activity.

To the Editor:Idiopathic inflammatory myopathies (IIMs) are a diverse group of rare and refractory systemic autoimmune diseases. DNA methylation, influenced by both inherited DNA sequences and environmental exposure, is a critical epigenetic factor that regulates gene expression by modifying the transcriptional chromatin accessibility of regulatory sequences within genes.^[1,2,3]To explore potential pathogenic mechanisms and identify accessible biomarkers for dermatomyositis (DM) and polymyositis (PM), we conducted a comprehensive analysis of alterations in both the DNA methylome and transcriptome in peripheral blood from patients with DM and PM. Additionally, we examined the serum profiles of inflammatory cytokines/chemokines.

To the Editor: Essential tremor (ET) is a common movement disorder with significant clinical heterogeneity.^[1]Following the proposal of "ET-plus", the cross-sectional investigation of ET has increased. However, the characteristics of pure ETvs. ET-plus remain unclear. Herein, we present a longitudinal follow-up study of pure ET and ET-plus patients that aimed to clarify disease progression and outcome, to determine the annual incidence rates of pure ET to ET-plus, and ET to Parkinson’s disease (ET-PD), and to investigate the clinical biomarkers influencing disease outcomes.

To the Editor: Chimeric antigen receptor (CAR)-T-cell therapy has made considerable breakthroughs in the treatment of lymphoma and myeloma, but the lack of suitable or specific targets for acute myelocytic leukemia (AML) has limited the progress of CAR-T-cell therapy in the clinical treatment of AML. Cluster of differentiation (CD)312, a member of the adhesion G protein-coupled receptor family, is highly expressed in acute myeloid leukemia and absent in normal hematopoietic stem cells (HSCs),^[1]making it a potential target antigen for CAR-T-cell therapy. In this study, we assessed the expression of CD312 in AML cell lines and patients and constructed anti-CD312 CAR-T cells, which showed excellent antitumor activity and safetyin vitroandin vivo. Notably, CD312 CAR-T cells exhibited no significant off-target effects, suggesting their potential as an effective and safe treatment strategy for AML.

To the Editor: After chimeric antigen receptor T (CAR-T) cell therapy, over 90% of patients experience either mild or severe cytopenia, with the prevalence of Grades 3–4 neutropenia ranging from 53% to 94.3%.^[1,2]Granulocyte colony-stimulating factor (G-CSF), known for its ability to enhance the proliferation and differentiation of neutrophils, has been extensively employed for the prevention and treatment of neutropenia in various contexts. However, its application in patients with refractory/relapsing B-cell acute lymphoblastic leukemia (R/R B-ALL) after CAR-T cell therapy remains a topic of debate.^[3]Several studies have suggested that G-CSF may exert anti-inflammatory effects by modulating the release of inflammatory factors, such as interleukin-12 (IL-12), TNF-α, and IFN-γ, or by influencing the differentiation of T-cell subsets.^[4]However, other researchers have posited that G-CSF could exacerbate cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) through the augmentation of antigen-presenting cell function. Moreover, the severity of ICANS has been found to be strongly associated with elevated levels of serum G-CSF in B-ALL.^[5]To provide a basis of knowledge for this topic, further research is warranted, which should include additional clinical and experimental studies of G-CSF and evaluation of the impact of G-CSF on CRS and ICANS in the content of B-ALL. This comprehensive information will enable clinicians to make more informed decisions when formulating treatment strategies for patients. We, therefore, conducted a retrospective analysis of 168 R/R B-ALL patients who developed neutropenia within one month after receiving CD19 CAR-T cell therapy at Tianjin First Central Hospital from June 2017 to December 2022. Informed consent for participation in this clinical trial (registered at www.chictr.org.cn as ChiCTR-ONN-16009862 and ChiCTR1800015164) was obtained from all patients and their families at Tianjin First Central Hospital. This study was approved by the Ethics Committee of Tianjin First Central Hospital (No. 2015002X), and the relevant clinical trials fully adhered to the principles outlined in theDeclaration of Helsinki. Among these patients, 89 patients received G-CSF at a dose of 2.5–5.0 mg·kg⁻¹·day⁻¹during neutropenia (G-CSF group) and 79 patients did not receive G-CSF (control group). Overall survival (OS) was defined as the duration from CAR-T cell infusion to death from any cause. Progression-free survival (PFS) was defined as the period from CAR-T cell infusion to disease progression or death. Statistical analyses were conducted using SPSS Statistics 26.0 (IBM Corp, Armonk, NY, USA) and GraphPad Prism 9.0 (GraphPad Software, CA, USA).

To the Editor:Autologous CD19 chimeric antigen receptor (CAR) T-cell therapy has emerged as a crucial treatment option for patients with relapsed or refractory diffuse large B-cell lymphoma (r/r DLBCL).^[1]While CAR-T-cell therapy has the potential for curing a subset of patients despite its high cost, over 60% of recipients eventually experience relapse.^[2]This troubling statistic has led several clinical centers to investigate the underlying reasons for CAR-T-cell therapy failure or suboptimal outcomes.^[3,4]Currently, a reliable method for predicting the curative efficacy of CAR-T cells is lacking.^[5]In this study, we conducted a comprehensive analysis to identify various predictors influencing the success of CAR-T-cell therapy. Our efforts have culminated in the development of a predictive model designed to assess the therapeutic efficacy of CAR-T-cell therapy.

To the Editor: Graft-versus-host disease (GVHD) is a rare but fatal complication after solid organ transplantation (SOT), with an incidence of 0.2–2.0%. Recent retrospective studies have shown a mortality rate of approximately 85–98% among patients with SOT-GVHD.^[1]Various drugs and methods have been shown to improve or alleviate clinical symptoms, but no effective treatments for GVHD currently exist. Recent clinical experience with SOT-GVHD treatment is mixed and limited, including systemic or partial corticosteroid support, the use of Janus kinase (JAK) inhibitors, allogeneic hematopoietic cell transplantation (alloHCT), and donor-targeted serotherapy. Since the number of lymphocytes transplanted with the organ may be a risk factor for GVHD, reducing the number of donor lymphocytes seems beneficial. Intensity-modulated radiation therapy (IMRT) is a type of radiotherapy that uses optimized, non-uniform radiation beam intensities on the patient.^[2]Local allograft irradiation has also been used to treat severe resistant rejection after liver transplantation (LT) in previous studies.^[3]Based on this, we hypothesized that whole-liver IMRT at a low dosage could be used as a rescue therapy to control acute GVHD after LT by reducing the number of donor-derived immune cells.

To the Editor: Refractive disorder (RD) is an initiative undertaken so as to eliminate avoidable blindness by 2020 (VISION 2020: the Right to Sight).^[1]It is one of the most common causes of visual impairments worldwide. Uncorrectable RD is the main cause of visual impairment in children and adolescents.^[2]Thus, RD, especially myopia, has a high impact on economic costs and adds to the burden of visually disabling age-related complications in adulthood.^[3]In China, RDs are also a public health issue. Current epidemic studies provide the characteristics of refractive errors among Chinese children and adolescents,^[4,5]while national-level data on the epidemic characteristics of RDs and the disease burden are still unknown. This study assessed the burden of refractive errors in all the provinces across China among Chinese children and adolescents younger than 20 years over the past three decades.

In the article "UBE2C affects breast cancer proliferation through the AKT/mTOR signaling pathway" published in Vol. 134, Issue 20, pages 2465–2474 ofChinese Medical Journal,^[1]the authors admit that they misplaced the pictures in the procedure of organizing the figure. The error does not affect the results and conclusions of the article. The updated and correct Figure 3 is shown below. The authors deeply apologize for any inconvenience caused.