APOE and myocardial infarction: Van den Doncket et al. reported that Fbn1C1039G/+ mice crossed with atherosclerosis-prone ApoE deficient mice (ApoE−/−:Fbn1C1039G/+) died suddenly, and elastin fragmentation led to intraplaque neovascularization, plaque rupture, myocardial infarction, and stroke in ApoE−/−:Fbn1C1039G/+ mice [58].