In vivo studies using genetically modified mice—including KO, knockdown, and transgenic models—have implicated the roles of individual Cldns (Cldn1 to 5, 7, 11, 14, 16, 18.1, 18.2, and 19), revealing alterations in TJ barrier or paracellular channel functions associated with various pathological conditions such as inflammation, cancer, metabolic disorders, and deafness (2, 34). Here, CLDN1 is linked to metabolic disease.