These concerns suggest that TGF-β may originate from AMs/metaplastic type 2 alveolar epithelial cells and concurrent SARS-CoV-2 infection in patients with IPF, and the resultant damage to alveolar tissue from acute COVID-19 may allow for TGF-β to spill into the bloodstream for prolonged periods of time and instigate pulmonary vascular remodeling that can ultimately lead to the development of PAH (Fig 2). Here, TGFB1 is linked to idiopathic pulmonary fibrosis.