Further analysis of BBS resulted in development of BBS knockout mice (Bbs2, Bbs4 and Bbs6) that developed hyperphagia, reduced energy expenditure and increased circulating leptin levels, which suggests that leptin deficiency is not the mechanism of obesity in BBS (Rahmouni et al., 2008). The gene discussed is BBS2; the disease is obesity due to melanocortin 4 receptor deficiency.