The pathophysiology of irAEs involves the development of autoimmunity, including the release of auto-reactive T cells and generation of pre-existing auto-reactive antibodies, the on-target attack of shared tumor antigens on normal tissue, target tissue expression of immune checkpoints (e.g., CTLA-4 on normal pituitary), and inflammatory cytokine release (e.g., IL-17 and colitis). This evidence concerns the gene CTLA4 and neoplasm.