Mutations in the KRAS gene directly trigger the EGFR-Ras-Raf-MAPK pathway in the EGF signaling pathway, followed by activation and overexpression of MAPK1 to further promote tumor cell migration and invasion, increase cell viability and participate in epithelial mesenchymal transition, allowing the rapid progress of LUAD and rendering targeted drugs against the EGFR upstream pathway ineffective (Lee et al., 2014). The gene discussed is KRAS; the disease is neoplasm.