Specifically, homozygous loss-of-function (LoF) mutations in genes such as LEP, LEPR, and homozygous and heterozygous in MC4R result in uncontrollable hyperphagia, an eating disorder characterized by excessive hunger and food intake, leading to extreme early-onset obesity [5, 20]. This evidence concerns the gene LEP and obesity due to melanocortin 4 receptor deficiency.