In this study, we set out to characterize the cellular expression, regulation, and function of ALK4 in subcutaneous and visceral adipose tissues through gain- and loss-of-function experiments using ligand activation and ALK4-deficient primary adipocytes, respectively, as well as in vivo studies in mouse strains lacking ALK4 expression from different stages of adipocyte differentiation subjected to diet-induced obesity. The gene discussed is ACVR1B; the disease is obesity due to melanocortin 4 receptor deficiency.