Contrarily to CRP, PTX3 is produced at sites of inflammation, by resident and inflammatory cells, such as myeloid and epithelial cells, lymphatic and vascular endothelial cells, smooth muscle cells, and fibroblasts [12]; evidence shows that PTX3 is also expressed and released by adipose tissue, with a possible interaction of this modulator with both atherosclerosis and obesity [13, 14]; PTX3 does not respond to IL-6 stimulus, like CRP, but, instead, its expression is induced by lipoproteins, by the proinflammatory stimulus of TNF-α, and by the activation of Toll-like receptors [12, 15]. The gene discussed is CRP; the disease is obesity due to melanocortin 4 receptor deficiency.