Considering the observation that re-expression of wild-type EPHA3 in H1299 cells increased apoptosis by suppression of AKT activation in vitro [19], as well as that the AKT/mTOR pathway was upregulated in SCLC, and inhibiting mTOR signaling with RAD001 potently disrupted growth and survival signaling in human SCLC cells [47], we proposed the hypothesis that the upstream gene of AKT, PI3K, may be involved in apoptosis of SCLC cells. This evidence concerns the gene AKT1 and small cell lung carcinoma.