Genetic ablation of the hematopoietic AMPK β1 subunit has been shown to increase adipose tissue macrophage infiltration and inflammatory markers and to reduce rates of fatty acid oxidation [8], while increased AMPK activity enhances lipid metabolism and anti-inflammatory actions in the liver and macrophages, offering protection against diet-induced obesity and the insulin resistant phenotype [9,10,11]. This evidence concerns the gene PRKAA1 and obesity due to melanocortin 4 receptor deficiency.