Collectively, these findings indicate that KRAS mutations drive immune evasion in colorectal cancer through multifaceted mechanisms, including CXCL3-mediated MDSC recruitment via IRF2 suppression, PD-L1 downregulation in MSI-H tumors, and CTLA-4-dependent Treg expansion, ultimately dampening anti-tumor CD8+ T-cell responses and immune escape (46). This evidence concerns the gene KRAS and neoplasm.