To date, the exact mechanism of the development of irAEs has yet to be elucidated, and potential mechanisms may include enhanced T cells activity against antigens present on tumor and normal tissues; increased concentrations of pre-existing autoimmune antibodies; increased levels of inflammatory cytokines, CTLA-4 antibody directly binding to normal tissues expressing CTLA-4 (such as pituitary gland), thereby promoting the enhancement of complement-mediated inflammatory response (Passat et al., 2018). The gene discussed is CTLA4; the disease is neoplasm.