A putative mechanism by which ANGPTL4 might evoke endothelial dysfunction involves hyperglycemia, as suggested by an investigation showing that the genetic ablation of ANGPTL4 in mouse adipose tissue not only improves glucose tolerance, but also reduces atherosclerosis [37], hence underscoring the relevant influence of ANGPTL4 on both glucose metabolism and vascular disease. The gene discussed is ANGPTL4; the disease is atherosclerosis.