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. This evidence concerns the gene LEPR and Obesity.