In addition, contrary to what was observed in normal cells, in cancer cells, the upregulation of ACLY concurs to maintain a low cytosolic level of citrate, favoring further the enhancement of glycolysis (which would be inhibited by high citrate) and the activation of oncogenic drivers, such as the PI3K/Akt and WNT/β-catenin pathway, which promotes aggressiveness, EMT and de-differentiation [77,87,91,144,145,149]. This evidence concerns the gene ACLY and cancer.