Higher tumor mutation burden (10- to 50-fold) and more neoantigens in MSI-H tumors, together with higher levels of multiple checkpoints, including PD-1, cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), and lymphocyte activation gene 3 (LAG3) in MSI-H tumors, may explain in part why anti-PD-1 treatment works more efficiently in MSI-H CRCs than in MSS CRCs [15,16]. This evidence concerns the gene PDCD1 and neoplasm.