A shift from an antiinflammatory (M2) adipose tissue macrophages (ATM) to pro-inflammatory (M1) ATM and promotion of IL-17 producing T-helper (Th)-17 cells through transforming growth factor (TGF)-β and IL-6 along with the stabilization of Th17 cells by IL-23 contribute to the proinflammatory state of obesity [21]. This evidence concerns the gene IL17A and obesity due to melanocortin 4 receptor deficiency.