In the context of inflammation-induced insulin resistance seen in obesity, the subcellular localization of these DUSPs may be a critical point of difference, with serine phosphorylation of IRS1 by various serine kinases including ERK1/2 and JNK thought to be a key effector mechanism by which pro-inflammatory stimuli induce cellular insulin resistance [1]. The gene discussed is IRS1; the disease is obesity due to melanocortin 4 receptor deficiency.