By contrast, PD-1 blockade was reported to be effective against microsatellite instability–high/MMR-deficient (MSI-H/dMMR) CRCs, with a response rate of 30%–70%, which can be explained by the high tumor mutation burden (TMB), potentially becoming tumor neoantigens (8, 10, 11), although MSI-H/dMMR accounts for approximately 10% of CRCs (12). Here, PDCD1 is linked to neoplasm.