Additionally, ABCs exacerbate chronic inflammatory microenvironments by activating senescence-related signaling pathways (e.g., mTOR/NF-κB), promoting abnormal activation and tissue infiltration of autoimmune cells (e.g., Th17), ultimately accelerating the pathological progression of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and related disorders [140]. The gene discussed is NFKB1; the disease is rheumatoid arthritis.