This suggests that TGFβ1-induced upregulation of TG2 is likely to be regulated by both canonical (SMAD3) and non-canonical (ERK) TGFβ1-induced signalling which may explain why 60% knockout of SMAD 3in IPF fibroblasts only gave rise to around 25% decrease in TG2 expression when compared to control cells. Here, SMAD3 is linked to idiopathic pulmonary fibrosis.