Other studies on CK2 in cells resistant to apoptosis support the implication of the NF-κB pathways: its attenuation has been considered a major mechanism for the reversal of Cisplatin resistance induced by CK2-blockade [30], and it has been demonstrated to be reduced, together with EGFR expression, in CK2-inhibitor treated glioblastoma and pancreatic adenocarcinoma cells resistant to conventional chemotherapy [22]. This evidence concerns the gene NFKB1 and glioblastoma.