This was supported by our results wherein TGF-β1-induced mLFs (the primary mLFs), C3H/10T1/2 Clone8 cells (the mouse fibroblasts) and the WI38 cells (the human fibroblasts) showed increased protein levels of lung fibrosis markers, while both knockdown or pharmacological inhibition of DOT1L reduced collagen deposition and expression levels of fibrosis markers in response to TGF-β1, supporting that DOT1L regulated the TGF-β1-induced fibrosis in vitro. Here, TGFB1 is linked to pulmonary fibrosis.