The altered site due to the −146 C > T mutation specifically involves non-canonical NF-kB signaling with cooperative binding between p52/RelB and ETS1 rather than general binding of the multimeric GABPA/GABPB1 complex as reported in gliobastoma, liver and bladder cancer cell lines29,43–45. The gene discussed is NFKB1; the disease is urinary bladder cancer.