Consistent with the notion of attaining therapeutic efficacy by co-targeting of the PI3K/AKT/mTOR/CK1α signalling axis and 26 S proteasome, recent studies have shown that pharmacological inactivation of PI3K or mTOR enhances the sensitivity of cancer cells to Bortezomib and overcomes Bortezomib-induced resistance.76, 77, 78. The gene discussed is AKT1; the disease is cancer.