Standing the PKCθ/CYLD antagonism, we can hypothesize that the PKCθ hyperactivation observed in N3-ICtg thymocytes may suppress the CYLD function, thus further sustaining NF-κB activation, in agreement with Notch/Hes1-induced CYLD repression and reduced expression of this IKK negative regulator in primary T-cell leukemia (85). Here, NFKB1 is linked to T-cell leukemia.