FAS and cancer: In this setting, cancer cells chronically exposed to extracellular acidosis (due, for example, to excess protons secreted by glycolytic cancer cells that saturate bicarbonate buffer) would reprogram their metabolism, arresting glycolysis (proton H+ is a well-known inhibitor of PFK1 [8,51]), and enhancing reductive carboxylation of glutamine sustaining FAS and promoting FAO [109].