Considering the aforementioned effect of CHC on MM cell energy levels and hexokinase II expression, it is plausible that CHC-induced ATP paucity contributes to reduced (ATP-dependent) BCRP function under these treatments, as suggested by our previous work showing that inhibition of glycolysis by 3-bromo-pyruvate suppresses ATP production and restores drug sensitivity in BCRP-expressing RPMI8226 cells as well as p-glycoprotein-expressing KG1 leukemia and HepG2 hepatoma cells [29]. This evidence concerns the gene ABCB1 and hepatocellular carcinoma.