To better elucidate the role of the PI3K/AKT/mTOR pathway in MeCDDA-induced apoptosis in lung cancer cells, we transfected an AKT cDNA which can constitutively express the AKT protein to H1688 cells and treated these AKT over-expressed cells with MeCDDA, measuring the cell viability to quantify the results. This evidence concerns the gene MTOR and lung carcinoma.