IGF1 and metabolic dysfunction-associated steatotic liver disease: The authors suggest a “two-programming” hypothesis for the augmented risk of NAFLD in the case of prenatal alcohol exposure, in which the “first programming” consists of the intrauterine programming of liver glucose and lipid metabolic function and the “second programming” is led by postnatal adaptive catch-up growth triggered by intrauterine programming of glucocorticoid-IGF1 axis.