Consistent with this implication, the results of IPA analysis suggest that the cancer-selective, growth-suppressive effect of ACR in inhibiting the ATP production of HCC cells may be related to a putative PDK4-dependent molecular signaling mechanism involving RXR and PPARs, as has been reported in certain fatty acid signaling pathways [42] (Figure 7B). This evidence concerns the gene PDK4 and hepatocellular carcinoma.