It might be speculated that targeting one of the driving forces of HB tumorigenesis, namely the constitutive activation of IGF2-PI3K-AKT survival signaling, which is not evident in most tumor models investigated so far,27, 40, 42, 43 in concert with other as yet unknown HB-specific inherent alterations that are targeted by CM-272, could have resulted in an antitumor effect that induces a systemic response that cannot be tolerated in vivo. Here, AKT1 is linked to neoplasm.