Lin et al. have shown that TNFi (ETN and ADA) not only suppressed proinflammatory IL-17 and IL-22 but also downregulated the acetylation of histones H3 and H4 in the RORγt gene promoter region of Th17-polarized cells from RA patients, suggesting a close link between biologic therapy on histone modification [179]. The gene discussed is ADA; the disease is rheumatoid arthritis.