In this view, Alms1 disruption generates a novel model which involves the pathological expansion of AT, typical of obesity models [43], [44] with a dramatic hyperinsulinemia, characterizing lipodystrophic models [45], [46] and suggesting that very high insulin levels could overcome a primary AT IR and drive its expansion to obesity. Here, ALMS1 is linked to obesity due to melanocortin 4 receptor deficiency.