KRAS and neoplasm: In addition to intrinsic signaling adaptations, alterations within the tumor microenvironment (TME)—including upregulation of immunosuppressive mediators such as IL-6 and PD-L1 (programmed death-ligand 1) or expansion of myeloid-derived suppressor cells (MDSCs)—can further promote immune evasion and therapeutic resistance, underscoring the multifactorial nature of resistance mechanisms in KRAS-mutant cancers [63,64,65,66].