Moreover, the circulating levels of sDPP4 were shown to be dissociated from the degree of systemic and AT inflammation [31], and this may explain why therapeutic agents modulating plasma DPP4 were not shown to protect from consequences of chronic low-grade inflammation, i.e., endothelial dysfunction and atherosclerosis, and from AT metabolic impairment in humans. The gene discussed is DPP4; the disease is endothelial dysfunction.