BDNF and obesity due to melanocortin 4 receptor deficiency: The severe obesity phenotype in a mouse mutant where the Bdnf gene is deleted in many brain regions using a Cre transgene under the control of the CaMKIIα promoter (Rios et al., 2001) has been widely cited as evidence for BDNF as an anorexigenic factor because the transgene starts to express Cre recombinase in the hippocampus during the third postnatal week, after many developmental events in the brain have already been completed (Tsien et al., 1996; Xu et al., 2000a).