Wild-type, Lrp8+exon19 and Lrp8Δexon19 mice were also mated with the atherosclerosis-susceptible Ldlr−/− mice to generate Lrp8WTLdlr−/−, Lrp8+exon19Ldlr−/− and Lrp8Δexon19Ldlr−/− mice to assess how apoER2 exon 19 splice variants may influence atherosclerosis progression. The gene discussed is LDLR; the disease is atherosclerosis.