Indeed, microsatellite instability alone may not be sufficient to predict response to immune-checkpoint inhibitors, as, for example, not all tumor neoantigens may bind the major histocompatibility complex (MHC) class I. Additional immune-regulatory mechanisms may have a role as a contributor of anti-PD-1/PD-L1 response, as T cell absence and genetic/epigenetic alterations [58]. Here, PDCD1 is linked to neoplasm.