Alterations in SLC6A4 expression have been associated with food intake and obesity in animals and humans; transgenic mice overexpressing SLC6A4 are lighter and shorter than controls [33], whereas SLC6A4 knockout mice develop late onset obesity, hepatic steatosis, glucose intolerance, and insulin resistance [34–36]. The gene discussed is SLC6A4; the disease is obesity due to melanocortin 4 receptor deficiency.