Accordingly, the present study aimed to exploit the modulation of tumor-mitochondrion energy metabolism by affecting the EGFR/HERs/PI3K/AKT/mTOR pathway with miR-125 as an adjuvant therapy combined with Afa, a potent EGFR-TKI-targeting the broad-spectrum ErbB family, in a prospective nanoparticle formulation for potential GC therapy. The gene discussed is AKT1; the disease is neoplasm.