Furthermore, they showed that the emerging apoptosis-resistant phenotype of IPF-derived fibroblasts is probably due to the aberrant regulation of PTEN/Akt axis, which inactivates FoxO3a, resulting in the downregulation of caveolin-1 suppressing the Fas expression in IPF-derived fibroblasts cultured on polymerized collagen [108]. The gene discussed is FAS; the disease is idiopathic pulmonary fibrosis.