SR-B1-KO mice containing atherogenic mutations in either apoE (KO or hypomorphic) or LDLR (LDLR-KO) develop either spontaneous (in the case of SR-B1/apoE double KO) or HFC diet-induced (in the case of SR-B1-KO/hypoE or SR-B1/LDLR double KO mice) coronary artery atherosclerosis, myocardial infarction, and dramatically reduced survival (Braun et al., 2002, 2003; Zhang et al., 2005; Karackattu et al., 2006; Nakagawa-Toyama et al., 2012; Al-Jarallah et al., 2013; Fuller et al., 2014; Hermann et al., 2016; Luk et al., 2016; Liao et al., 2017). The gene discussed is LDLR; the disease is coronary atherosclerosis.