We demonstrated that sFasL inhibits T-cell-induced apoptosis in IPF lung fibroblasts [6], in contrast to the role of mFasL in the cytotoxicity of CD4+ T-cells, which ensures their escape from immune surveillance [7], survival and proliferation in vitro, and in vivo in the experimental lung fibrosis and air pouch models [6]. The gene discussed is FASLG; the disease is idiopathic pulmonary fibrosis.