Although the development of experimental lung fibrosis in wild-type mice is inhibited in the absence of canonical TGF-β/Smad3 signalling (Bonniaud et al, 2004; Zhao et al, 2002), the protective effect arising from its ablation is overcome in situations of excessive Stat3 activation that results from mutant gp130757F receptors during bleomycin-induced lung injury or from the sustained presence of IL-6 family cytokines, including Osm. This evidence concerns the gene STAT3 and pulmonary fibrosis.