Apoptosis requires the complex interplay of many signaling molecules, and the deficiency or overexpression of other apoptosis regulatory proteins besides Fas has also been implicated in the resistance of fibroblasts to apoptosis in the setting of pulmonary fibrosis.14, 15 In fact, our finding that Fas expression is diminished in fibroblasts from bleomycin-injured mice differs from that of Wallach-Dayan et al.,7 who did not observe a difference in Fas expression between fibroblasts from bleomycin-injured mice and controls. The gene discussed is FAS; the disease is pulmonary fibrosis.