However, because TGF-β is a potent chemical mediator of lung fibrosis, with prior studies showing that Tregs promote fibrosis via TGF-β-associated mechanisms, the effect of Lck inhibition in the present study to reduce TGF-β production by Tregs [49] may be advantageous for lung fibrosis, regardless of the timing of treatment. Here, TGFB1 is linked to pulmonary fibrosis.