Overexpression of p22phox (NOX membranal subunit) in vascular smooth muscle led to ROS overproduction and an increased tendency to develop signs of the metabolic syndrome in mice.45 NOX1 was also shown to be expressed in vascular smooth muscle cells, and its mRNA expression was upregulated and activated by vascular pathological stimuli, such as Ang II and PDGF.46, 47, 48 It is reasonable to speculate that the aASC signature stems from the physiological tendency of vascular cells within the fat abdominal tissue to overproduce ROS in an NOX-dependent manner. The gene discussed is NOX1; the disease is metabolic syndrome.