Furthermore, in some cases, the effects of NRF2 are complex and cell type-specific, such as in a mouse model of atherosclerosis, where loss of NRF2 in bone marrow-derived cells exacerbates atherogenesis, but loss of NRF2 overall increases plaque inflammation and vulnerability, thereby reducing lesion development (Gao et al., 2013; Zhong et al., 2017). This evidence concerns the gene NFE2L2 and atherosclerosis.