We also treated silica exposed C57BL/6 mice with a pharmacologic inhibitor (BAY 11-7085) of NFKBIA (IκBα) phosphorylation [14] or exposed transgenic mice expressing a dominant negative NFKBIA (IκBα) mutant protein [15], [16] under the control of epithelial specific promoters mice to silica to determine whether the systemic or epithelial inhibition of NF-κB activation is a valid therapeutic approach in silicosis. The gene discussed is NFKBIA; the disease is silicosis.