NFKB1 and bacterial infectious disease: As Drice levels are increased upon bacterial infections, the Drice-Diap2 complex described earlier (Fig. 4), might, besides regulating Diap2 and NF-κB-mediated immune signalling [24], also play a role in maintaining homeostatic cell turnover by restraining excessive Drice activity, and apoptosis-mediated cell proliferation during steady-state conditions.