Metabolic syndrome may be related to the development of hypertension via complex pathways including an increase in angiotensin II via adiposity-induced inflammation and a decrease in NOS activation via oxidative stress and insulin resistance.[37] The two mechanisms are probably intertwined in coexisting hyperuricemia and metabolic syndrome, in which the effect of hyperuricemia on uncontrolled BP might be undetectable, as shown in our study. The gene discussed is AGT; the disease is hyperuricemia.