In the setting of malignancy, anti-programmed cell death protein ligand 1 (PD-L1) binds to PD-1, enabling cancer cells to evade host immune surveillance.[4] Anti-CTLA-4 and anti-PD1 checkpoint blockade therapies target distinct tumor-infiltrating T-cell populations to induce tumor rejection.[5]. The gene discussed is CTLA4; the disease is neoplasm.