Immune cells play pivotal roles in iridocyclitis, with effector T lymphocytes, particularly Th1 and Th17 subsets, significantly contributing to disease severity.[6,7] Th1 cells produce IFN-γ, driving macrophage activation and tissue damage, while Th17 cells release IL-17, perpetuating chronic inflammation and tissue remodeling.[8,9] Activated macrophages further exacerbate inflammation through the secretion of pro-inflammatory cytokines and reactive oxygen species, contributing to oxidative stress and subsequent damage to retinal and choroidal tissues. The gene discussed is IL17A; the disease is iridocyclitis.