In this respect one of the reason might be found in the simultaneously inactivation of Ras/Raf/extracellular signal-regulated kinase (ERK) pathway and the activation of the phosphoinositide3-kinase (PI3K)/protein kinase B (Akt) / mammalian target of rapamycin (mTOR) in tumor cells as well as CTCs. This evidence concerns the gene AKT1 and neoplasm.