FasL expression is tightly regulated and induced by NF-kβ.[33] Tumor-expressing FasL was destroyed by infiltrating granulocytes observed in vivo, considered being involved in the pathogenesis of autoimmune disease.[34, 35] In silicosis patients, apoptosis is initiated when Fas is engaged by Fas trimers. The gene discussed is NFKB1; the disease is silicosis.