However, in the case of EGFR-mutant H1975 NSCLC cells (L858R and T790M positive), our study suggests that alternative EGFR signaling may be occurring mainly through the MAP Kinase and/or PI3K/Akt-stimulated mTOR pathway, resulting in cancer cell proliferation and survival. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.