Cancer immunotherapy targeting inhibitory molecules such as the programmed cell death receptor 1 (PD-1) or ligand 1 (L1) axis or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) (collectively referred to as immune checkpoint molecules) has improved outcomes across many cancer types1,2; however, treatment may be suboptimal3,4. This evidence concerns the gene CTLA4 and cancer.