Currently described non-syndromic forms of mendelian obesity comprise mainly genetic defects in the leptin/melanocortin pathway, such as mutations in the genes encoding LEP, LEPR, prohormone convertase 1 (PC1/3), proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R), leading to overeating [79,83]. The gene discussed is LEP; the disease is obesity disorder.