We focused on the induction of apoptosis by this compound because p53-dependent apoptosis is a critical mechanism for preventing lymphomagenesis 33, 34 and determines the outcome of lymphoma treatment.35 In NALM6 cells, MMRi64 at 1 μM showed a time-dependent induction of PUMA, a critical pro-apoptotic downstream gene product of p53.36, 37 Interestingly, p21, the growth-arresting effector target gene of p53, was transiently induced then downregulated to a level lower than basal p21 expression at 24 h of the treatment. The gene discussed is TP53; the disease is lymphoma.