Considering the adult onset obesity in the mutant mice [27], the reduced melanocortinergic tone in N2KO mice [24], [26], and the expression patterns of Nhlh2 in the hypothalamus and spinal cord, we hypothesized that a targeted deletion of Nhlh2 would result in a disruption of the Mcr to adipose tissue outflow, leading to defects in adipose tissue metabolism. The gene discussed is NHLH2; the disease is Obesity.