One patient sample demonstrated high levels of Smad3 binding to the ITGB6 promoter compared with other donor tissue tested, raising the possibility that aberrant Smad3 binding could be one of multiple possible molecular defects that contribute to variations in αvβ6 expression in IPF, and highlights the potential for heterogeneity in the molecular mechanisms driving disease in IPF patients. Here, SMAD3 is linked to idiopathic pulmonary fibrosis.