Therefore, EGFR TKIs can achieve potent antitumor activity in EGFR-mutant NSCLC by preventing HER3/PI3K/AKT signaling activation.54 Even during ongoing EGFR-TKI therapy, HER3 can be activated by binding with an amplified MET oncogene, and this can perpetually activate the PI3K/AKT pathway.55 Thus, as a result of these characteristics of HER3 and its activity in cell survival signaling pathways, it might be a promising therapeutic target in EGFR-mutant NSCLC. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.