Previous studies reported that IFITM3 served as a PIP3 scaffold engaged to amplify PI3K/AKT signaling in B cells [23], while activation of MET via binding to HGF was found to enhance cancer cell proliferation, metastasis as well as resistance to regimens like chemotherapies through triggering of downstream PI3K/AKT signaling [31–33]. The gene discussed is AKT1; the disease is cancer.