T-cell checkpoint inhibitors, in particular, such as those that target programmed cell death protein 1 (PD-1), its ligand PD-L1, or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), are responsible for the majority of immunotherapy successes in cancers such as melanoma and lung cancer; other cancer types exhibit lower numbers of responders with these drugs, which could be due to the lack of T-cell infiltration or (neo)antigen expression.2 Manipulating a cancer patient’s own T cells has solidified the concept that immune cells can be targeted effectively for patient benefit. This evidence concerns the gene CTLA4 and lung cancer.