This was recently determined by the generation of hyperlipidemic ApoE−/− mice lacking ERV1/ChemR23, which exhibit exacerbated atherosclerosis with larger lesions containing more macrophages compared with ERV1/ChemR23 expressing ApoE−/− littermates (Laguna-Fernandez et al., 2018). The gene discussed is APOE; the disease is atherosclerosis.