Studies show that upon activation of mTOR, the downstream S6K can phosphorylate insulin receptor substrate 1 (IRS-1), reducing the activity of PI3K and, through negative feedback, attenuating the activity of the PI3K/Akt/mTOR pathway, thereby inhibiting tumor cell activity (Leiphrakpam and Are, 2024). This evidence concerns the gene AKT1 and neoplasm.