Moreover, we demonstrated that this adipose-specific phenotype can be recapitulated in vitro, and that the in vivo phenotype is robust and does not present in a bistable fashion as does the global haploinsufficient model, challenging the previous paradigm that Trim28-induced obesity primarily stems from alterations in developmental cellular lineages. This evidence concerns the gene TRIM28 and obesity due to melanocortin 4 receptor deficiency.