TNFAIP3 and hereditary disease: Several human genetic diseases confirm the multifunction of NF-κB including genetic defects in NF-κB activating molecules (e.g., NEMO) resulting in an immunodeficiency phenotype (Döffinger et al., 2001; Pannicke et al., 2013) and in NF-κB regulatory molecules (e.g., A20/TNFAIP3, OTULIN) which causes an autoinflammatory phenotype (Damgaard et al., 2016; Zhou et al., 2016).