Since then NF-kB/BCL3 signaling has been reported to be responsible for glioma resistance to temozolomide through upregulation of the extrinsic apoptosis inhibitory decoy receptor DcR1 which blocks apoptotic responses via Fas/TRAIL [121], and BCL3-dependent upregulation of the carbonic anhydrase II (CAII) gene via a temozolomide mediated switch between p50/BCL3 and p52/BCL3 complexes at the CAII promoter [92]. This evidence concerns the gene NFKB1 and glioma.