The binding of PD-L1 to its receptor PD-1 on activated T cells reduces antitumor immunity by lowering T cell proliferation, cytokine production, and cytotoxic capacity.[9] In many types of cancer, CTLA-4 is an important negative regulator of T cell responses, eventually resulting in T cell fatigue and T cell malfunction.[10,11] CTLA-4 inhibition can boost antitumor T-cell immunity.[12] ICIs targeting CTLA4, PD-1, and its ligand PD-L1 have shown considerable promise in clinical trials for a range of malignancies, including metastatic melanoma, NSCLC, and renal cell carcinoma (RCC). The gene discussed is CTLA4; the disease is cancer.