Immune checkpoint blockade (ICB) therapy has proven to be a transformative treatment option for a variety of cancers.1, 5 By blocking inhibitory receptors, most commonly programmed cell death protein-1 (PD-1), programmed death-ligand 1 (PD-L1) or cytotoxic T-lymphocyte associated protein 4 (CTLA-4), T cell function is improved, thereby enabling these cells to more effectively combat a patient’s tumor.6, 9 Even though the clinical benefit of ICB is unprecedented, the majority of patients fail to respond durably to this treatment, because of several types of resistance.5 10 11. This evidence concerns the gene CTLA4 and cancer.