LDLR and atherosclerosis: A potentially important mouse model of human atherosclerosis with elevated LDL-C is one in which both the Ldlr and Apobec1 genes are deleted (Ldlr−/−/Apobec1−/−, hereafter referred to as L−/−/A−/−), since these mice lack the ability to convert apoB-100 to apoB-48 in liver and also are defective in LDL clearance.