 Growth hormone-releasing hormone, GHRH, is a key regulator of TH17 cell differentiation and plays a crucial role in the development of autoimmune ocula and neural inflammation. GHRH signaling induces the activation of the Janus kinase, signal transducer, and activator of transcription 3, JAK, a stat 3 pathway, which leads to increased phosphorylation of stat 3 and the subsequent upregulation of genes associated with pathogenic TH17 cell differentiation. This signaling also suppresses the expression of genes associated with non-pathogenic TH17 cells. Increased GHRH signaling can therefore promote the development of pathogenic TH17 cells and lead to the progression of autoimmune ocula and neural inflammation. This article was authored by Lin Du, Bo Man Ho, Lin Bin Du, and others.