Taken together, these results demonstrate that FoxO3a regulates IPF fibroblast viability at least, in part, via cav-1 and that abnormally low FoxO3a protects IPF fibroblasts from polymerized collagen induced apoptosis via suppressing cav-1/Fas-dependent pathway. The gene discussed is CAV1; the disease is idiopathic pulmonary fibrosis.