These data, coupled with the aforementioned data suggesting Cldn10-positive cell migration, provide insights into the mechanism of fibrosis initiation in nonfibrotic alveoli in IPF, i.e. a plausible scenario wherein club cells with profibrotic properties randomly migrate and get attached to an alveolar wall, and subsequently interact with and activate the fibroblasts in the subjacent alveolar interstitium. Here, CLDN10 is linked to idiopathic pulmonary fibrosis.