Furthermore, ALCAT1-targeted inactivation prevents diet-induced obesity and nonalcoholic fatty liver disease (NAFLD) and neurotoxin1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) induced neurotoxicity, reduces oxidative stress injury, improves mitochondrial function, and mitigates apoptosis [19, 20, 23]. Here, LCLAT1 is linked to obesity due to melanocortin 4 receptor deficiency.