Indeed, hypoxia induces AEC2 proliferation via increased doxycytidine kinase (DCK) expression in the lung epithelial cells of IPF patients.10 Although little is known about the protein kinase function of DCK, it has been recently shown to increase pFAK1 levels,39 which strengthens our observation of FAK1 as a central regulator of epithelial hypoxia signaling. The gene discussed is WEE1; the disease is idiopathic pulmonary fibrosis.