Apart from the ionizing irradiation that contributes to the development of pulmonary fibrosis by directly activating EMT in type II alveolar epithelial cells, fibrotic formation was largely driven by the abnormal release of fibrosis facilitators, such as TGF-β1, α-SMA, TNF-α, IL-1bβ and IL-6, after exposure to high doses of ionizing radiation2,4,32. Here, ACTA1 is linked to pulmonary fibrosis.