Thus, early genetic studies of severe obesity (SevO) focused on identifying gene-disrupting mutations in the leptin-melanocortin pathway (e.g., LEPR, MC4R, POMC) [37–41], which are linked to early-onset SevO through dysregulation of food intake and food preferences [42]. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.