TNF-α, IL-17, and IL-10 are central players in RA’s immune regulation [39]: TNF-α, a primary proinflammatory cytokine, induces the secretion of VCAM-1 and ICAM-1 and stimulates the production of IL-6, IL-8, and GM-CSF [40], while IL-17 exacerbates inflammation and bone erosion by promoting bone resorption and vascular opacity [41]; in contrast, IL-10 modulates B cell functions and antibody production, with its in vivo concentration negatively correlated with the susceptibility and severity of RA [42]. The gene discussed is IL10; the disease is rheumatoid arthritis.