In this study, we show that FoxO3 is a crucial player in driving IPF fibroblast phenotype by performing experiments in human IPF tissue, human ex vivo‐cultured fibroblasts of healthy and IPF lung origin and a mouse model of lung fibrosis with employment of global‐ and fibroblast‐specific FoxO3 knockout mice. This evidence concerns the gene FOXO3 and pulmonary fibrosis.