Interestingly, experimental studies on mouse models with orexin deficiency [46, 47] reported both a modulatory effect of the hypothalamic orexin system on respiratory activity [48], and an increase in spontaneous sleep apnoeas, especially in REM sleep [49], thus suggesting that the orexin dysfunction found in PWS may partly contribute to the pathophysiology of sleep-breathing disorders, commonly present in this syndrome. This evidence concerns the gene HCRT and Prader-Willi syndrome.