KRAS and neoplasm: These include promoting tumor growth via the PI3K-AKT pathway through ROR1, especially in epidermal growth factor receptor (EGFR)-mutant LUAD [19], and suppressing tumor progression by upregulating adhesion-related genes (e.g., MYBPH, OCLN, CLDN1, CLDN18) and inhibiting the epithelial-mesenchymal transition and KRAS-driven mucinous transformation [20–24].