Further investigations using brain specific and inducible FTO deficiency or FTO deficiency tied for example to certain hypothalamic (e.g. CRH) neurons may be useful for (i) revealing the precise neurobiological pathways underlying the autonomic phenotype of FTO deficient mice and (ii) determining whether reducing the expression or inactivating catalytic activity of FTO might represent a promising strategy to purse in order to alleviate obesity. This evidence concerns the gene CRH and obesity disorder.