Additionally, the interaction of follistatin with the main pro-inflammatory cytokines in RA, including TNF-α, IL-1β, and IL-6 (released by both fat cells and muscle cells), may promote a chronic inflammatory state within skeletal muscle, exacerbating intermuscular fat infiltration, impairing muscle function, and contributing to muscle atrophy and weakness [15,16]. The gene discussed is FST; the disease is rheumatoid arthritis.