Indeed, previous research has suggested that PSAT1 induced the protein level of Cyclin D1 through modulating the GSK3β/β-catenin axis, contributing to accelerated cell cycle in breast cancer.41 Moreover, it has been indicated that PSAT1 could interact and activate pyruvate kinase M2 (PKM2), an enzyme that controls the final and rate-limiting reaction during the glycolysis pathway, leading to metabolic alterations and subsequent tumor growth.42 However, instances of the moonlighting function of PSAT1 in sensing the glucose concentrations and orchestrating metabolic switch are rare. This evidence concerns the gene PKM and breast carcinoma.