Liao et al. (2019) demonstrated that KRAS∗-mediated repression of IRF2 results in high expression of CXCL3, which binds to CXCR2 on myeloid-derived suppressor cells and promotes their migration to the tumor microenvironment, which drives immune suppression and immune therapy resistanc in CRC. Our results suggest a positive correlation (r = 0.31, P < 0.0001) between the mRNA expression levels of CXCL3 and CD274, which encodes PD-L1, and a negative correlation (r = −0.17, P < 0.0001) between the mRNA expression levels and the abundance of infiltrating cytotoxic T-lymphocytes. The gene discussed is CXCR2; the disease is neoplasm.