Tsujino and colleagues [57] reported decreased numbers of CD151-positive AECs in patients with IPF, although most AECs in normal lungs express CD151, indicating that a downregulation of this tetraspanin may play a role in the pathogenesis of IPF. In vitro, CD151-knockdown type II AECs exhibited attenuated adhesion on Matrigel, enlarged morphology, and increased α-SMA expression. The gene discussed is ACTA1; the disease is idiopathic pulmonary fibrosis.