Immune checkpoint inhibitors (CPIs) have transformed the treatment landscape for many cancers by inducing a durable survival benefit even after cessation of therapy.1–4 However, while inhibition of immune checkpoint molecules such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) potentiates an anti-tumor immune response, this immune activation comes at the cost of triggering immune-related adverse events (irAEs) that can target virtually any organ system. The gene discussed is CTLA4; the disease is cancer.