The roles of fenestration and permeability of LSECs in liver diseases have drawn more attention in recent years.[22, 44] The disorder of substance exchange between blood and hepatic parenchyma leads to the development of liver‐related metabolic diseases.[17] In fact, some previously reported phenotypes of Cavin1−/− mice, such as glucose intolerance and hyperinsulinemia, are metabolically related to liver functions.[45] The novel function of Cavin1 in regulating the fenestration of LSECs may partially contribute to the phenotypes in Cavin1 knockout mice. This evidence concerns the gene CAVIN1 and Hyperinsulinemia.