In mouse models of obesity, macrophages switch from an anti-inflammatory M2 phenotype (producing IL-10) to a pro-inflammatory M1 phenotype, which overexpress inflammatory cytokines including IL-6 and TNF-α32 and are likely to be a major contributing source of these cytokines in adipose tissue. This evidence concerns the gene IL6 and obesity due to melanocortin 4 receptor deficiency.