In summary, our preclinical data suggest that blockade of the NF-κB pathway with Bortezomib could render CRC more sensitive to BET inhibition in vitro and in vivo, through repression of FOXM1 to induce G2/M arrest, and repression of c-myc expression to subsequently increase GADD45 proteins and anti-angiogenic factors CTGF and Tsp-1 (Fig. 6f). The gene discussed is CCN2; the disease is colorectal carcinoma.