However, deletion of Nrf2 in myeloid cells of LDL receptor knockout mice (LDLr-/-) exacerbates atherosclerotic lesions and increases pro-inflammatory genes expression (Collins et al., 2012), indicating that Nrf2 activity in myeloid cells and macrophages modulates the pro-inflammatory vascular milieu associated with atherosclerosis. The gene discussed is LDLR; the disease is atherosclerosis.