Rheumatoid arthritis and other autoimmune diseases are chronic inflammatory diseases that seriously endanger human health and affect quality of life, and there is still a lack of curative therapies for these diseases. Therefore, there is great interest in the study of the mechanism of inflammatory autoimmune diseases, hoping to provide new mechanisms, new targets and new directions for the development of drugs for the prevention and treatment of this disease. In recent years, it has been found that abnormal histone modifications are closely associated with the pathogenesis of major human diseases, such as tumors, cardiovascular diseases, and autoimmune diseases, and are gradually becoming a popular new target for disease diagnosis and treatment. To this end, the study was carried out by linking epigenetic modifications, inflammation and natural immune response regulation, and autoimmune disease development mechanism. Through small RNA interference universal screening experiments, Xia Meng and Liu Juan, PhD students from the Institute of Immunology, Zhejiang University School of Medicine and the State Key Laboratory of Medical Immunity, Second Military Medical University, found that among the 14 H3K4(de)methylation transferases screened, H3K4 methylation transferase Ash1l could significantly negatively regulate the production of interleukin 6, an inflammatory cytokine triggered by pathogen stimulation, in macrophages. In collaboration with Xiaohui Wu and Tian Xu, professors at the Institute of Developmental Biology, Fudan University, they further found that older Ash1l-deficient mice with more infiltrated inflammatory cells in their organs and high levels of interleukin 6 in their bodies were more prone to spontaneous autoimmune diseases with accompanying inflammatory damage in organ tissues. This suggests that Ash1l molecules can prevent the development of inflammatory autoimmune diseases.