Downregulation of AKT to increase apoptosis is one of the many ways to address the neuroblastoma tumor growth, and two main strategies are being pursued: (1) long-term exposure of SH-SY5Y cells to interferon β, which decreased activation of the P13K-AKT pathway [43,44], thereby increasing the apoptosis, and (2) Rapamycin-induced mTOR (a downstream effector of AKT) inhibition [45], which is related to decreased tumor growth, angiogenesis, and increased apoptosis. Here, AKT1 is linked to neuroblastoma.