The MK signaling pathway exhibited significant functional heterogeneity across different tumor types: In cervical cancer, this pathway synergistically promoted HPV-related progression through ECM remodeling mediated by cancer-associated fibroblasts and immunosuppression (83); in hepatocellular carcinoma, it promoted angiogenesis and metastasis, and coupled lipid metabolism to drive immunosuppression (84); and in lung adenocarcinoma, it collaboratively drove tumor progression with EGFR signaling and induced T cell rejection (85). Here, EGFR is linked to neoplasm.