CHKB and muscular dystrophy: The many-fold decrease in the expression of these Ppars that was specific to affected muscle, along with their coreceptors and downstream target genes corroborate the lipidomics data that suggest that the major change in lipid metabolism in Chkb mediated muscular dystrophy is an inability to metabolize fatty acids via mitochondrial β-oxidation resulting in shunting of excess fatty acid into TG rich lipid droplets.