Furthermore, the relationship between NOX4 and mitochondrial oxidative stress in aging atherosclerosis was supported by substantially increased colocalization of immunoreactive NOX4 with mitochondrial marker ATP5G in brachiocephalic artery sections from aged Apoe-/- mice (a 3.3-fold increase over young Apoe-/- mice; Figure 3B). The gene discussed is APOE; the disease is atherosclerosis.