This phenomenon seems to be dependent on several mechanisms in different cancers: aberrant IKK activity, a shorter half-life of IκB in B-cell lymphoma, mutated IκB in Hodgkin’s lymphoma, IL-1β production in acute myelogenous leukaemia, TNF production in cutaneous T-cell lymphoma and Burkitt’s lymphoma [21,22]. This evidence concerns the gene TNF and primary cutaneous T-cell non-Hodgkin lymphoma.