Moreover, we have shown that Bbs4 plays a role in the ER stress induced in early cell differentiation in vitro in both adipocytes and neuronal cell models [252,253], highlighting that BBS obesity is not only an outcome of a decreased satiety but is mediated in part by peripheral mechanisms, such as accelerated hyperplasia and hypertropia, and the dysfunction or abnormalities of adipocytes. This evidence concerns the gene BBS4 and obesity due to melanocortin 4 receptor deficiency.