Biologically, KRAS mutations have been associated with a pro-inflammatory tumor microenvironment mainly via higher PD-1/PD-L1 expression, CD8+ tumor-infiltrating lymphocytes (TILs) and TMB [87,88,89], and other data also demonstrated that PD-L1 expression is higher in KRAS mutant versus wild-type cases (PD-L1 in KRAS mutant vs. wild-type: 65.3% vs. 58.5%, p = 0.0002) [90]. Here, CD8A is linked to neoplasm.