Furthermore, we show that tumours lacking Stat3 showed increased nuclear p-p65 concomitant with increased expression of CXCL1 and other typical NF-κB target genes, such as Tnfα, c-Myc and Il-6, which was also shown by others in A549 cells as well as in glioblastoma cells upon STAT3 blockade59, 60. The gene discussed is STAT3; the disease is glioblastoma.