Given the indications that Etv5 is involved in obesity and given its presumed role in dopaminergic signaling, we here further characterize the role of Etv5 in the etiology of obesity, by determining whether Etv5 stimulated the TH promoter, whether expression of Etv5 in VTA is regulated by leptin and whether overexpression of Etv5 affects body weight, food intake and/or the motivation to work for a sucrose pellet. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.