Several mechanisms of EGFR-TKIs acquired resistance are involved in progression of NSCLC, including T790M mutation, upregulation of MET/HGF, HER2 mutations, overexpression of HER3, persistent activation of IGF-1R, mutations of PIK3CA/AKT, and abnormal dimerization of STAT3 5, 6. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.