Consistent with this finding, Ad-Smads2/3/4 infection stimulated hepatic fatty acid utilization by stimulating the oxidation of fatty acids via mitochondrial and peroxisomal β-oxidation pathways in a MPK38 phosphorylation-dependent manner, whereas Smad7 had the opposite effect on fatty acid utilization (Fig. 6d). Here, SMAD7 is linked to infection.