Apart from the ionising irradiation contributing to the development of pulmonary fibrosis by directly activating EMT in type II AECs, fibrotic formation is largely driven by the abnormal release of fibrosis facilitators, such as TGF-β, CTGF, TNF-α, IFN-γ, IL-1β, and IL-6, after exposure to high doses of ionising radiation3, 25, 27. Here, CCN2 is linked to pulmonary fibrosis.