These results, although very preliminary, coupled with previous findings that attribute variants in the FTO gene to increased food intake [3], [19] and increased FTO mRNA translation [36] suggest that alterations in the transcriptional status in FTO may contribute to obesity by disrupting neuronal cellular energy status, and altering the signaling mechanisms that are responsible for controlling energy intake. Here, FTO is linked to obesity due to melanocortin 4 receptor deficiency.