FIGURE 1.

Schematic representation of the pathogenesis of RA. Both MHC region genes and non‐MHC region genes contribute to genetic susceptibility of RA, with HLA‐DRB1 most attributable. Epigenetic alterations participate the development and progress of RA through DNA methylation, histone modification, chromatin remodeling, RNA modification, and ncRNAs. In the immune microenvironment of RA, many pathologic cell subtypes are identified, which might be novel treating targets in the future. Metabolic disorders of glucose, lipid, and amino acid are also found in different cells in rheumatoid joints.