NR4A1 was identified as a previously unrecognized constitutive regulator of adipocyte progenitor (AP) quiescence.296 In ex vivo experiments, NR4A1 gain-of-function reduced adipogenesis, whereas its loss-of-function increased adipogenesis.296 Compared with control mice, NR4A1 knockout mice fed a high-fat diet were more prone to obesity, with increased gene expression of PPARγ and FAS. The gene discussed is NR4A1; the disease is obesity due to melanocortin 4 receptor deficiency.