Anti-CTLA4 treatments exacerbate existing colitis in mouse models that employ irritants which induce intestinal epithelial damage such as dextran sodium sulfate, but no model to date has demonstrated that anti-CTLA4 treatment can drive intestinal inflammation de novo.21 22 Deletion of CTLA-4 during adulthood leads to autoimmune disease in mice23; therefore, we hypothesized that prolonged CTLA-4 neutralization might mimic irAE observed in clinic. This evidence concerns the gene CTLA4 and autoimmune disease.