Even if heterozygous carriers of deleterious mutations in MC4R, POMC, LEP and LEPR present a milder and incompletely penetrant form of obesity in comparison with the obligatory severe obesity phenotype caused by homozygous / heterozygous compound loss of function mutations in the same genes, they are likely to contribute for a non-negligible fraction of obesity at the population level. Here, LEPR is linked to obesity due to melanocortin 4 receptor deficiency.