However, the absence of NRF2 in HFD myeloid-derived macrophages [120] or the deletion of Nfe2l2 in myeloid cells of LDL receptor KO mice [121] aggravates atherosclerotic lesions and increases pro-inflammatory genes expression, indicating that NRF2 modulates the pro-inflammatory vascular milieu associated with atherosclerosis. This evidence concerns the gene NFE2L2 and atherosclerosis.