In NSCLC, AKT activation may result from distinct and often mutually exclusive events that include activating mutations or increased expression of one or more of AKT isoforms (AKT1, AKT2 or AKT3) or of their upstream regulators such as KRAS or PIK3CA or loss of negative regulators (i.e. PTEN) [8, 31]. This evidence concerns the gene PIK3CA and non-small cell lung carcinoma.