Indeed, we and others have previously demonstrated that T cells with a genetic inactivation of Th17 cell regulating transcription factors retinoic acid-related orphan receptor gamma t (RORγt), interferon regulatory factor-4, signal transducer and activator of transcription 3 (STAT3), or basic leucine zipper transcription factor ATF-like (BATF) uniformly failed to induce colitis in a series of syngeneic murine IBD models supporting the concept that harnessing unleashed intestinal inflammation can be achieved by targeting Th17 cell biology (7–11). The gene discussed is STAT3; the disease is inflammation.