Urao and Ushio-Fukai [27] demonstrated that hindlimb ischemia increases Nox2-dependent ROS production in isolated bone marrow-derived mononuclear cells (BM-MNCs) and that postischemic neovascularization and mobilization of BM cells (BMCs) are impaired in Nox2 knockout mice concluding that Nox2-derived ROS regulate progenitor cell expansion and reparative mobilization in response to ischemia. This evidence concerns the gene CYBB and ischemia.