Interestingly, a recent study, by Dabiri et al.32, showed that p53-null colorectal cancer cells were transiently resistant, in the first 24 h, to the proteasome inhibitor bortezomib, whereas becoming responsive after 48 or 72 h of treatment, when the oncosuppressor isoform of p73, TAp73, translocated and accumulated in the nuclei of treated cells. The gene discussed is TP53; the disease is colorectal cancer.