Cancer acquires mechanisms to escape the immune system during development and progression.1 2 One such mechanism involves the induction of inhibitory molecules, such as programmed death 1 (PD-1)/PD-1 ligands and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4).1–4 Immune checkpoint inhibitors (ICIs) against these molecules improve the outcome of various types of cancer including melanoma and lung cancer.5–7 However, their efficacy as monotherapy is unsatisfactory, with a response rate of less than 50%. This evidence concerns the gene CTLA4 and lung carcinoma.