As lung fibrosis involves proliferation of the activated MYF, it is logical to conclude that MYF exists in two different configurations: the “synthetic” MYF that are highly proliferative, undifferentiated, and that deposit high ECM and the “contractile” MYF that are not proliferative and that express the terminal differentiation marker αSma. Here, ACTA1 is linked to pulmonary fibrosis.