Furthermore, this signaling pathway might serve as a backup to compensate increased PI(3,4,5)P3 levels in the plasma membrane, e.g., in PI3K gain of function or PTEN loss of function mutations, which occur in various types of cancer: increased PI(3,4,5)P3 enhances the activation of PDK1/Akt, which in turn results in the activation of mTOR [57], which is counterbalanced by simultaneous activation of LKB1/AMPK and subsequent inhibition of mTOR by AMPK [58,59]. This evidence concerns the gene PDK1 and cancer.