The tumour suppressor p53 exerts its effects by regulating transcription of various genes required for cell cycle control, apoptosis and DNA repair. Its close relative p73 is also a transcription factor, but some splice forms lack a transactivation domain (e.g. ΔNp73α) and thus might play an antagonistic role. The extent to which the regulatory circuits involving p53 and p73 - particularly ΔNp73α - overlap is unclear. Sétha Douc-Rasy and co-workers have therefore examined their interplay in malignant neuroblastoma cells, in which p53 is sequestered outside the nucleus (see p. 293). Surprisingly, they observe that both full-length p53 (TAp73α) and ΔNp73α stabilize p53 protein. However, TAp73 causes p53 to return to the nucleus; ΔNp73α does not. The authors also observe that TAp73 and ΔNp73α have differential effects on genes downstream of p53 - TAp73 induces expression of the apoptosis protein PUMA, for example, but ΔNp73α does not. In each of these cases, the effect requires wild-type p53. By contrast, TAp73 can stimulate synthesis of the cell cycle inhibitor p21 even when endogenous p53 is mutated. These results indicate that p73 can have p53-independent effects but that, frequently, the regulatory pathways involving the proteins overlap, and the truncated ΔNp73α plays a repressive role.