To attack the metabolic benefit gained by cancer cells due to VDAC1-bound HK, many compounds designed to interfere with glycolysis by targeting HK, such as by 2-deoxyglucose (2-DG) and 3-bromopyruvate (3-BP), that also targets GAPDH, and lonidamine (a derivate of indazole-3-carboxylic acid), were developed [47, 48]. This evidence concerns the gene GAPDH and cancer.