IL-17A expression is significantly increased in RA, with Th17 cells isolated from RA joints expressing higher levels of RANKL; moreover, Th17 cells can induce the production of inflammatory factors such as TNF-α, IL-1β, and IL-6, and have the ability to induce the expression of RANKL on FLS, indirectly contributing to the generation of osteoclasts [50,51]. The gene discussed is IL1B; the disease is rheumatoid arthritis.