AKT1 and neoplasm: Additionally, it could disrupt Hsp90 (heat shock protein 90) and Cdc37 (cell division cycle 37) interaction [9] by binding to the C-terminal domain of Hsp90; it could also induce apoptosis in multiple tumor cells by activating c-Jun N-terminal kinase and suppressing PI3K/Akt (Phosphatidylinositol-4,5-bisphosphate 3-kinase/Protein kinase B) signaling pathways [10].