The recent review series on interstitial lung disease has created a great deal of interest. However, the review by Williams and Wilson of novel treatments and lung transplantation in pulmonary fibrosis1 does not reflect recent developments in clinical and translational research in idiopathic pulmonary fibrosis (IPF).

The belief that inflammation is the primary driver of fibrosis in IPF has been superseded by newer pathogenetic paradigms that emphasise the role of aberrant wound healing in the evolution of fibrosis.2 The pathogenetic importance of inflammation has been downgraded. Furthermore, greater diagnostic accuracy has led to a better understanding of IPF disease behaviour. It is now appreciated that patients with IPF may have periods of …