Increased circulating concentration of vaspin during insulin resistance in obesity can be explained by its compensatory mechanism, targeting adipose tissues and antagonizing the disrupting effects of unknown proteases in insulin action [44], such as the inhibitory effect on human kallikrein (hK7) that mediates the degradation of insulin in circulation [45]. The gene discussed is KLK4; the disease is obesity due to melanocortin 4 receptor deficiency.