IKBKB and neoplasm: Even so, on the basis of all available data on DTP3 and results from the abovementioned genetic models, including the recent observation that myeloid-specific Gadd45b loss potentiates tumour-associated inflammation via a JNK-unrelated mechanism, any potential pro-inflammatory effects of DTP3 are expected to be both mild and localised, rather than systemic and dose-limiting, as in the case of IKKβ inhibitors [7,[32], [33], [34], [35]], and therefore most likely manageable with anti-inflammatory treatment.