While IGF2BP2 has been reported to drive the progression of NASH through elevating hepatic iron deposition and increasing production of hepatic-free cholesterol.73,74 In contrast, global IGF2BP2 deficiency prevents mice from NAFLD by causing resistance to obesity and fatty liver, whereas hepatocyte-specific deletion of IGF2BP2 promotes moderate diet-induced fatty liver through impairing FA oxidation by increasing mRNA degradation of PPARα and carnitine palmitoyltransferase 1A which were supposed to be stabilized and bound by IGF2BP2.75 This evidence concerns the gene PPARA and metabolic dysfunction-associated steatotic liver disease.