In TP53/KRAS co-mutant non-small cell lung cancer (NSCLC), Mtp53 enhances tumor immunogenicity and improves response to immune checkpoint inhibitors (ICIs); conversely, in immunologically "cold" tumors-such as triple-negative breast cancer, pancreatic ductal adenocarcinoma, and colorectal cancer-it promotes T-cell exhaustion or myeloid suppression, reflecting marked cancer-type heterogeneity. This evidence concerns the gene KRAS and neoplasm.