In addition to an effect on glycolytic metabolism, ARS inhibited HCT116 colon cancer cell proliferation by suppressing the fatty acid biosynthetic pathway, mainly downregulating three proteins: acyl-CoA synthetase 5, hydroxyacyl-coenzyme A dehydrogenase and fatty acid synthase [54,59,60]. This evidence concerns the gene HADH and malignant colon neoplasm.