Another finding that supports the idea that there is no deficient transport of leptin through the BBB is that of the Bardet-Biedl Syndrome (BBS) mouse model, characterised by retinal dystrophy, polydactyly, renal and gonadal anomalies, cognitive impairment, and obesity, and, where proteins of an octameric complex, the “BBSome”, are mutated, leading to impaired transport of the leptin receptor LepRb to the plasma membrane in hypothalamic cells, thereby preventing intracellular signalling which causes resistance to leptin and obesity [82]. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.