Activation of NF-κB involves alterations of RelA (p65) and NF-κBB2 (p100/p52) and has been implied in inflammatory liver injury and hepatocarcinogenesis, as well as in the context of STZ-induced diabetes.20, 21, 22 In response to STZ treatment, the expression of p100 and p52 increased with a trend toward higher levels in flip−/− mice compared with wt. The gene discussed is NFKB1; the disease is diabetes mellitus.