Despite tumor mutation load as the primary driver of microsatellite instability in CRC, other mechanisms do exist, such as the high expression level of PD-L1 (programmed death-ligand 1) and close association between tumors expressing PD-L1 or PD-L2 (programmed death-ligand 2) and immune infiltrates (Taube et al., 2014; Salem et al., 2018). The gene discussed is CD274; the disease is neoplasm.