DOT1L and pulmonary fibrosis: On the basis of these observations, TGF-β1-induced DOT1L upregulation might lead to increase the abundance of H3K79 trimethylation at the promoter region of the Jag1, further binding to the Notch1 receptor and releasing the NICD to translocate into the nucleus, modulating the profibrotic gene expression and accelerating the lung fibrosis.