In this perspective, it could be interesting to study the hypothesis that at least in a subgroup of subjects with ASD during the life there may be an initial excess of activity of the hypocretinergic system (to which the problems of insomnia are fundamentally correlated), followed by a normalization of this system or even, more rarely, by a sort of exhaustion leading to a deficit/absence of hypocretin with the possible appearance of narcoleptic symptoms. This evidence concerns the gene HCRT and insomnia.