To explore the potential mechanism(s) underlying alcohol-induced TRPC3 downregulation in hepatocytes and the liver, several pathways, including oxidative stress, endoplasmic reticulum (ER) stress, mitogen-activated protein kinases (MAPKs), hypoxia-inducible factor-1α (Hif-1α), nuclear factor erythroid 2-related factor 2 (Nrf2), etc., which have been documented to implicate in alcohol-induced hepatic steatosis [16–19], were screened using multiple specific chemical inhibitors. This evidence concerns the gene HIF1A and fatty liver disease.