The mechanisms of hepatic failure induced by ICIs are unclear but may include the following three factors: (1) over‐activated T cells attacking healthy liver tissue; (2) increased inflammatory cytokines, such as interleukin (IL)‐1a, IL‐2, and interferon (IFN)‐α2, disrupting the homeostatic immunity; and (3) increased autoantibodies contributing to a phenomenon similar to autoimmune hepatitis (AIH), with the difference that autoantibodies are generally low or negative.11 Here, IL1A is linked to autoimmune hepatitis.