This contradicts the successful combination of anti-PD-L1/CM-272 in a bladder cancer model (28) and of anti-PD-1/UNC0642 (G9a inhibitor) in the parental B16F10 model (68), as well as other preclinical reports on G9a or DNMT inhibition across different tumor models (8, 69, 70), and yet can be explained by diverse immune contextures or pharmacokinetics of epigenetic remodeling. The gene discussed is PDCD1; the disease is neoplasm.