MAF1 and obesity due to melanocortin 4 receptor deficiency: The liver-specific phenotype of the NML knockout coupled with differences in nucleotide consumption between Pol I and Pol III (∼60% vs. 15% in growing cell populations) argues that a knockout of Maf1 in any single tissue is unlikely to generate the full complement of phenotypes or provide the same level of protection against diet-induced obesity as the whole-body knockout.