Tauber and coworkers, who published the first study demonstrating that hyperghrelinaemia starts early in life, prior to hyperphagia and obesity [39], concluded for an impaired development of the ghrelin system in subjects with PWS, starting with excessive UAG, which then decreases, followed by an excessive increase in AG and a relative deficit in UAG. This evidence concerns the gene GHRL and obesity due to melanocortin 4 receptor deficiency.