In autoimmune diseases like rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), inflammatory signals such as TNFα and IL-6 lead to epigenetic reprogramming of SEs, resulting in the aberrant overexpression of pro-inflammatory cytokines such as TNF, IL1 family, and chemokines (11, 67). This evidence concerns the gene IL1B and rheumatoid arthritis.