Very recently, sustained phosphatidylinositol 3‐kinase (PI3K) activation has been shown to increase lung fibrosis by modulating the macrophage polarization.5 Although PI3K and STAT3 proteins represent two distinct cellular regulatory systems, a functional link between these two systems has been shown by the observation that a specific inhibitor of PI3K reduces the level of STAT3 phosphorylation.6 Thus, it is assumed that PI3K can tune macrophage phenotype at least in part by STAT3 translocation; however, the exact role of PI3K/STAT3 signalling on macrophage skewing remained unknown. This evidence concerns the gene STAT3 and pulmonary fibrosis.