The CTLA-4 inhibitors, by inactivating intratumoral and intestinal CTLA-4 + Treg cells, may promote the activation of effector T cells, such as cytotoxic T- lymphocytes (CTLs), resulting in the development of ICI colitis.43 However, in these patients, Treg cells do not tend to be reduced; these cells usually show gene expression related to an interferon (IFN)γ-mediated pro-inflammatory Th1-type effect.42 Indeed, increased levels of IFNγ and TNFα, the cytokine TNF-like 1A (TL1A) and its receptor DR3 are commonly found.44 This evidence concerns the gene IFNG and colitis.