These findings described above suggest that TGF-β1-induced DOT1L upregulation might lead to increase the abundance of H3K79 trimethylation at the promoter region of Jag1, promoting Jag1 gene transcription and binding to the Notch1 receptor, further releasing the NICD to translocate into the nucleus, modulating the profibrotic genes expression and accelerating the lung fibrosis. This evidence concerns the gene DOT1L and pulmonary fibrosis.