TNFAIP3 and neoplasm: This activation can result from interactions with the tumor microenvironment7–9 or as a result of somatic mutations affecting NF-κB family members or upstream signaling components, such as CD79B, BIRC3, CARD11, MYD88, TNFAIP3/A20, or inhibitors of kappa B (IκBs; refs. 3,5,6,10–13).