The Etiology Research Laboratory currently has 7 staff members (1 senior-level, 1 associate senior-level, 5 mid-level) and 4 doctoral and master's degree candidates. It has successively undertaken projects such as the Ministry of Science and Technology's 973 Program, the 863 Program, the National Natural Science Foundation of China's Major Research Plan, and Major International Cooperation Projects. It has received 8 National and Beijing Municipal Science and Technology Progress Awards, and 7 domestic and international invention patents. Over 150 papers have been published in journals including *Nucleic Acids Research* (2002), *Clinical Cancer Research* (2004, 2009, 2014), *PNAS* (2012, 2024), *Genome Biology* (2015), *EBioMedicine* (2015), *Molecular Cancer* (2020), *Oncogene* (2022), and *Chinese Medical Journal* (2024, 2025), with over 4,600 citations. The laboratory has also edited or co-edited 5 academic monographs. The laboratory has long been engaged in research on tumor etiology and epigenetics. It was the first to demonstrate that the human stomach can synthesize the N-nitrosoamide chemical carcinogen N-methyl-N-nitrosourea (NMU). It discovered that the protein encoded by the *SLC17A5* gene is a nitrate ion channel involved in non-enzymatic nitric oxide synthesis and the prevention of gastrointestinal stress injury. It identified a novel LncRNA gene, *P14AS*, on the antisense strand of the *CDKN2A* gene and elucidated its mechanism of action. It discovered a set of DNA methylation markers for gastric cancer metastasis. It found that *CDKN2A/P16* CpG island methylation can directly inhibit gene transcription, promoting immortalization and malignant transformation of normal human cells. It discovered and ultimately proved that *P16* CpG island methylation can be used as a predictive marker for malignant transformation of oral mucosal epithelial dysplasia. It identified a common deletion sequence in the *CDKN2A* gene and created a sensitive P16-Light assay method. Using this method, it was found that the *CDKN2A* gene exhibits both copy number deletion and amplification, which are closely related to the malignant transformation and regression of esophageal squamous epithelial dysplastic precancerous lesions, respectively, with significant clinical application potential. It revealed that RNA m6A methylation has an upstream regulatory network controlled by genes such as *TTC22*, *TTC7B*, and *TTC28*, influencing tumor development and progression. It discovered that *TTC28* plays a crucial role in maintaining genomic stability. Current main research directions: 1. Relationship between *CDKN2A/P16* gene copy number variation and tumor development and progression, and translational research: Exploring the relationship between *CDKN2A* gene copy number variation and nuclear deformation, and its application value in predicting malignant transformation of precancerous lesions and influencing the efficacy of CDK inhibitor therapy in tumors; investigating the intrinsic links between *P16* gene DNA methylation, chromatin conformation changes, and gene copy number variation. 2. Composition, function, and application research on the upstream homeostatic regulatory network of RNA m6A methylation levels: Exploring the roles and mechanisms of *TTC28* and *PCLAF* genes in controlling cellular RNA m6A homeostasis, cellular stress, and driving tumor development, progression, and drug resistance formation.