PI3K/Akt/mTOR pathway upregulation, with cytoplasmic phosphorylated Akt, occurs in 62% of neuroblastomas and is a promising therapeutic target (55, 56), due to the central role played by PI3K activation in stabilizing MYCN, rendering neuroblastoma tumors sensitive to PI3K inhibition via downregulation of MYCN and corresponding tumor proliferation (27, 57). This evidence concerns the gene AKT1 and neoplasm.