NFKB1 and hematologic disorder: Owing to the potential of the NF-κB suppressor function of A20, and given the link between tumorigenesis and NF-κB mediated chronic inflammation, the discovery of inactivation of A20 by genomic deletion, somatic mutation, or epigenetic hypermethylation in several types of hematological malignancies was not surprising [96,97,98].