In parallel, when a 300bp DNA fragment covering the putative p65 binding site in the MMP-9 promoter was cloned upstream to luciferase reporter gene and transfected into URGCP-overexpressing NSCLC cells and control cells, significantly increased luciferase activity was achieved by URGCP overexpression and the increased luciferase activity in URGCP-overexpressing NSCLC cells was markedly reversed by the dominant negative mutant of IκBα. The gene discussed is NFKBIA; the disease is non-small cell lung carcinoma.