In summary, the conclusion drawn by the experiments reported here is that mutant AKT1-E17K is an oncogene that can transform human immortalized lung epithelial cells and that the relocalization of the cyclin-dependent kinase inhibitor p27 is a key mediator of the oncogenic activity exerted by the E17K mutation of AKT1, with cytoplasmic relocalization of p27 being predictive of poorer prognosis in NSCLC patients. This evidence concerns the gene CDKN3 and non-small cell lung carcinoma.