Interestingly, genetic deletion of cldn18 results in (pathologic) epithelial regeneration efforts with alveolar enlargement, impaired barrier function, alveolar type-1 epithelial cell (AEC1) injury, AEC2 expansion and YAP activation, a proliferation/differentiation protein activated in IPF alveolar cells (68–70). The gene discussed is CLDN18; the disease is idiopathic pulmonary fibrosis.