As shown in pCan1 and pCan2 primary NSCLC cells, treatment with CC-115 (100 nM for 4 h) almost nullified phosphorylations of Akt (at the Ser-473 residue) and S6K (at the Thr-389 residue), suggesting that CC-115, the mTOR kinase inhibitor, indeed blocked both mTORC1 and mTORC2 activation (Fig. 4A). The gene discussed is AKT1; the disease is non-small cell lung carcinoma.