Given the essential role of STAT3 in Th17 cell differentiation and effector functions, proof-of-principle experiments showing that genetic ablation of STAT3 in T cells prevented development of EAU and EAE in mice [12], [13], provided impetus to develop drugs that target STAT3 pathways for treating uveitis and other autoimmune diseases mediated by Th17 cells. The gene discussed is STAT3; the disease is uveitis.