The increased plasma concentration of ClpB or its fragments allows a direct central effect at the hypothalamic level of stimulating the POMC-related satiating pathways [11] which in turn contribute to either the onset or the perpetuation of anorexia and hyperactivity which could be explain by a satiating and anxiogenic effects of ClpB mimicking α-MSH [19]. The gene discussed is CLPB; the disease is Anorexia.