OXT and morbid obesity: In keeping with the roles of oxytocin described in rodents (see below), patients with Prader–Willi syndrome (whose main characteristics are cognitive disabilities, chronic food craving, and morbid obesity) seem to present a deficit in the oxytocin producing neurons of the PVN (14), probably due to a loss of function or deletion of SIM1, a transcription factor controlling the expression of the OXT gene (15, 16).