Our results showed that GHRH-R signaling is essential for Th17 cell differentiation and Th17 cell-mediated autoimmune ocular and neural inflammation because the deficiency or inhibition of GHRH-R signaling resulted in (1) reducing non-pathogenic and pathogenic Th17 cell differentiation in vitro; (2) via suppressing the phosphorylation of STAT3 through JAK-STAT3 pathway; (3) impairing the pathogenicity of Th17 cells; and (4) suppressing autoimmune ocular and neural inflammation. This evidence concerns the gene STAT3 and inflammation.