For the in vivo studies, we elected to target POMC neurons since the obesity phenotype was largely recapitulated by disruption of the BBSome, though constitutive Bbs1 gene ablation, in these neurons.16 The use of inducible POMCCre mouse model allowed us to determine whether the obesity phenotype evoked by congenital BBSome deficiency is recapitulated by the disruption of this complex in adult stage. This evidence concerns the gene BBS1 and obesity disorder.