The latest data from clinical trials and preclinical mouse models suggest that the therapeutic inhibition of the PI3K–AKT–mTOR signaling network might have dual benefits: preventing tumor progression by suppressing proliferation, migration, and survival of cancer cells, and enhancing the tumor immune surveillance pathway and intrinsic antitumor immune characteristics by inhibiting the activation of immunosuppressants [47]. The gene discussed is AKT1; the disease is neoplasm.