Additionally, expression of another integrin, αvβ5, by airway smooth muscle cells has been proposed to be important in activating TGF‐β and promoting pathology in murine models of asthma.69 Hence, limiting the concentrations of bioactive TGF‐β by selectively targeting the integrins involved in its activation may represent a promising strategy by which to attenuate pulmonary fibrosis and asthma without compromising tolerance to innocuous antigens. The gene discussed is TGFB1; the disease is asthma.