It is also plausible that hyperglycaemia may contribute to IPF risk through key fibrotic pathways including disrupted DNA repair mechanisms, increased cellular senescence caused by increased oxidative stress and activation of transforming growth factor-β (TGF-β) signalling.8 9 The potential relationship between T2D and IPF is further complicated by metabolic factors becoming dysregulated both due to T2D and during T2D disease development. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.