Thus, although gene expression may be partially responsible for the increased levels of these enzymes in HCC, it is likely that their upregulation is predominantly due to factors relating to their transcription, translation and possibly degradation, most likely under the control of established oncoproteins such as KRAS [5] or lipid-activated transcription factors such as PPARδ [44,50]. This evidence concerns the gene KRAS and hepatocellular carcinoma.