CD4 and triple-A syndrome: In another study, the Notch γ-secretase inhibitor dibenzazepine (DBZ) clearly blocked Ang II-stimulated macrophage and CD4+ T cell accumulation in an Ang II-induced mouse model, simultaneously reversed Th2 response in vivo through Notch signaling, demonstrating the potential for DBZ as a new therapeutic agent for the treatment of AAA (72).