Similarly, identification of deficient MMR (dMMR)—whether due to Lynch syndrome or somatic inactivation—can predict sensitivity to programmed cell death-1 (PD-1) blockade across tumor types, a principle that extends to urothelial and prostate cancers with dMMR/microsatellite instability (MSI)-high biology [7,8]. This evidence concerns the gene PDCD1 and neoplasm.