Among the erlotinib-responsive lung cancer cell lines, we found that H1975 and H1650 cells were endowed with a lower degree of sensitivity to the drug compared with HCC827, in agreement with the previously demonstrated modulation of erlotinib response by lack of functional PTEN (H1650) or by the concomitant presence of the T790M EGFR resistance mutation (H1975) in these cells.38, 39, 40 This result suggested that an intact AKT inhibitory signaling (PTEN) is required for erlotinib-induced cytotoxicity of lung cancer cells with mutated EGFR. This evidence concerns the gene AKT1 and lung carcinoma.