We demonstrate that the combination of a FGFRi with an Akt inhibitor (Akti) was necessary to completely inhibit growth in FGFR-overexpressing EGFR-TKI-resistant NSCLC cancer cells both in vitro and in vivo, and furthermore that dual FGFRi and Akti exhibited a significantly stronger synergistic effect compared to targeting FGFR1 and EGFR. The gene discussed is EGFR; the disease is cancer.