ICI-induced arthritis mechanistically results from dysregulated T-cell hyperactivation, wherein the inhibition of regulatory checkpoints permits the activation of autoreactive T cells, leading to pro-inflammatory cytokine surges, including TNF-α, IL-6, IL-17, and VEGF-A, that recruit neutrophils, macrophages, and B cells to synovial tissues, ultimately causing joint damage and osteoclastogenesis in the absence of conventional autoantibodies such as RF or anti-CCP [88, 89, 91, 113, 114]. The gene discussed is IL17A; the disease is arthritic joint disease.