The results revealed that the absence of APOA4 influenced lipid decomposition (e.g., ACOX1, ACSL4, CPT1A, ACSL5, ACSL1, ACOX3, ACAA1, ACOX2, PPARα), synthesis (e.g., ANGPTL4 and PPARγ) and transport (e.g., APOA4, SCL27A4, PLTP, APOA1), and promoted the expression of PCK1, a key enzyme in gluconeogenesis, and PLIN2, a biomarker of lipid droplets.[42] These findings collectively implicate that the pronounced increase in APOA4 expression in IUGR males may represent a potential, protective mechanism against hypoxia. Here, ACSL1 is linked to fetal growth restriction.