For example, the core circadian molecule NPAS2 plays an important role in reprogramming glucose metabolism in HCC cells through upregulation of the glycolytic genes and downregulation of peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC-1α) expression; BMAL1 in the mouse liver increases fatty acid oxidation and partially reduces ethanol-induced fatty liver and liver injury through overexpression of the adipogenic transcription factor carbohydrate-response element-binding protein (ChREBP) [16–18]. This evidence concerns the gene BMAL1 and hepatocellular carcinoma.