ApoE and LDLR deficiency on the B6 background itself had different pathological features, as reviewed in the literature (Getz and Reardon, 2016); however, strikingly, we found that NOD Apoe−/− and NOD Ldlr−/− mice were both highly resistant to atherosclerosis, with 7-fold fewer plaques than the B6 Apoe−/− mice (Getz and Reardon, 2012). The gene discussed is APOE; the disease is atherosclerosis.