The distinct metabolic phenotypes of Lrp8+exon19 and Lrp8Δexon19 mice are in striking contrast to the metabolic phenotype of global Lrp8−/− mice, which displayed hyperglycemia but not hyperinsulinemia due to impaired insulin secretion, or bone marrow-specific apoER2-deficient mice, which exhibited hyperinsulinemia and hyperglycemia due to exacerbated tissue inflammation and inflammation resolution defects [11]. Here, INS is linked to hyperinsulinism.