PM-induced metabolic effects are, indeed, mediated at least in part by the downregulation of PPARα and their lipid metabolism-related target genes in the liver (i.e., Cyp4a14; Cd36; Slc27a1, solute carrier family 27 member 1) and in BAT (i.e., Ucp1, uncoupling protein 1), which favor hepatic steatosis and BAT whitening [194]. The gene discussed is UCP1; the disease is Hepatic steatosis.