This selectivity for the α subunit over the β subunit, both of which are catalytic and could homodimerize with NEMO to form a functional IKK, suggests that one way, cancer cells may escape the inhibition of NF-κB by DRAIC by expressing more IKKβ than IKKα (40, 41) or, in rare cases, by activating NF-κB by pathways independent of IKKα (42). The gene discussed is IKBKG; the disease is cancer.