Furthermore, fetuin-A has been implicated in the pathophysiological mechanisms that lead to obesity onset; indeed, this protein has been claimed to mediate the reduction of adiponectin synthesis through the modulation of the Wnt3a/PPARγ pathway, and has been proposed as a chemoattractant for macrophage recruitment and migration into adipose tissue, promoting their subsequent polarization to M1 pro-inflammatory subtype, that contributes mainly to the AT inflammation [16]. Here, PPARG is linked to obesity due to melanocortin 4 receptor deficiency.