The task is clear: we need better treatments for pulmonary fibrosis (PF). The two antifibrotic therapies licensed for idiopathic pulmonary fibrosis (IPF) have shown efficacy in other forms of PF but do not meet the needs of people living with PF; drugs that can halt or even reverse progression and, importantly, improve quality of life. Although a number of new potential therapies are now reaching late-stage clinical trials, the recent failure of three of these has been disheartening1 and highlights the need to dig deeper, and smarter, for new potential drug targets.

Over the last 9 years, several studies have shown that drug targets with support from genetic association studies were more likely to be successful in clinical development than those without.2–4 This has prompted considerable interest and investment in the generation of genetic data by academia and industry. The supposition underpinning the success of genetically supported targets is that they represent dysregulation of mechanisms that are causal of disease, rather than processes that are the consequence of disease. This is because the genetic perturbations that implicate genes in risk of development of a disease are fixed in an individual at conception and are not altered by subsequent lifestyle choices or environmental factors.

Genome-wide Association Studies (GWAS) for almost all complex …