While the existence of multiple mechanisms of TGF-β1 activation may be cell- and tissue-type dependent, complicating the adaption of a universal therapeutic strategy, pharmacologic inhibition of RGD-binding integrins attenuates renal fibrosis and improves organ function following injury (Basta et al., 2020) and antibody targeting of αvβ6 mitigates bleomycin-induced lung fibrosis (Horan et al., 2008). This evidence concerns the gene TGFB1 and pulmonary fibrosis.