Increased aerobic glycolysis [18] and sirtuin 1 (SIRT1) activity [19], reduced AMPK activity [18,20,21,22], mitochondrial dysfunction [18,23,24,25,26,27,28], enhanced reactive oxygen species (ROS) production [27], oxidative stress [24,27,29,30,31,32,33], lipid peroxidation [30,33], defective FAO [34,35], increased glutamine usage [36,37], and arginine auxotrophy [38] have been observed both in vitro and in vivo in animal models of ADPKD or in the tissues of patients with ADPKD. The gene discussed is PRKAA2; the disease is autosomal dominant polycystic kidney disease.