In skeletal muscle, the primary site of insulin-stimulated glucose disposal [3,4], the infiltration of certain immune cells and their paracrine interactions (crosstalk) with myocytes, and the ectopic lipid accumulation characteristic of obesity as a result of adipose tissue (AT) dysfunction contribute to the development of local and systemic insulin resistance [4,5,6,7]. Here, INS is linked to obesity due to melanocortin 4 receptor deficiency.