In fact, PI3K signaling is constitutively activated in NSCLC cells through inactivating somatic mutations in, or epigenetic silencing of, phosphatase and tensin homologue deleted from chromosome 10 (Pten), a lipid phosphatase that negatively regulates the PI3K signaling cascade [11]–[15]. This evidence concerns the gene PTEN and non-small cell lung carcinoma.