Thus, these data reveal that, once differentiated, all, or some, of the intestinal TH17 cells must continuously receive TGFβ signaling to sustain the TH17 cell program and not switch to a proinflammatory TH1 cell program, dependent on T-BET, leading to IFNγ production responsible for dsDNA damage in IECs and cancer development. Here, IFNG is linked to cancer.