Similarly in humans, SIM1 mutations seem to be involved in the pathogenesis of obesity; for example, a balanced translocation disrupting the SIM1 gene was found in a girl with severe non-syndromic early-onset obesity [5], and patients with 6q deletions encompassing the SIM1 gene present with Prader-Willi-like phenotypes including obesity and developmental delay [6]. This evidence concerns the gene SIM1 and obesity due to melanocortin 4 receptor deficiency.