17-DMAG inhibited protein levels of ALK, EGFR, and MET, even in the presence of ligand activation, and suppressed of AKT and ERK1/2 phosphorylation, thereby inducing apoptosis of ALK-rearranged NSCLC cells, irrespective of the presence of HGF or EGFR ligands. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.