We also found that promoter accessibility is increased significantly in the ApcΔ716Trp53R270H/R270H tumor cells, suggesting that the chromatin structures of gene promoters are opened by mutant p53, which may result in the wide activation of the Wnt/β-catenin and NF-κB pathways (Figure 2). The gene discussed is NFKB1; the disease is neoplasm.