AKT1 and neoplasm: Nevertheless, our data demonstrated that B56γ3 promoted EMT through upregulating AKT activity in CRC cells, suggesting that B56γ3 may act as a tumor suppressor or oncogene in a context-dependent manner such as tumors harboring aberrant B56γ3 overexpression and mutations causing hyperactivated PI3K/AKT (Fig. 4).