Li et al. (2014) confirmed that alcohol consumption is associated with a downregulation of PPARα activity, decreased mitochondrial β-oxidation, and the development of steatosis. The role of PPARα was emphasized by the exacerbation of ALD in Ppara−/− mice, as evidenced by increased markers of TG accumulation, inflammation, and fibrosis. Here, PPARA is linked to steatosis.