This immunomodulatory function manifests as a pro-cancer effect in various malignant tumors: in ER-negative breast cancer, the high expression of BST2 drives tumor cell migration and invasion [35]; in CRC, it promotes the formation of an immunosuppressive microenvironment by inducing the M2 polarization of tumor-associated macrophages (TAMs) [15]; in pancreatic cancer, BST2 binds to PD-1, activating the PI3K/AKT pathway, leading to the functional exhaustion and apoptosis of CD8+ T-cells [36]. This evidence concerns the gene AKT1 and pancreatic neoplasm.