We propose that this pathway provides a mechanism where activation of NF-κB, either as consequence of the tumor microenvironment or through mutation of upstream signaling pathways (such as occurs in a number of hematological malignancies [53]–[55]), can promote tumorigenesis in cells retaining wild type p53 by suppressing the consequences of p53 activation and providing a window during which further mutagenesis can occur. The gene discussed is NFKB1; the disease is neoplasm.