Similarly, mutations in KRAS, particularly G12C, could alter the tumor’s response to targeted therapies like EGFR-TKIs and MEK inhibitors by activating downstream MAPK and PI3K/AKT/mTOR pathways that promote tumor survival and drug resistance (Song et al., 2024; Ma X. et al., 2025). The gene discussed is AKT1; the disease is neoplasm.