While an increasing number of genetic loci causing Mendelian forms of obesity have been identified—including but not limited to leptin (LEP), proopiomelanocortin (POMC), melanocortin 4 receptor (MC4R) in early studies, and single-minded homolog 1 (SIM1), brain-derived neurotrophic factor (BDNF) and its receptor encoded by the neurotrophic tyrosine kinase receptor type 2 gene (NTRK2) in later studies [4–6]; these genetic loci are associated with morbid forms of obesity and explain only a small proportion of the observed obesity in populations. Here, LEP is linked to obesity disorder.