The p53 tumour suppressor is crucial for the ability of the cell to either arrest cell cycle progression or activate apoptosis in response to stimuli that may impinge on genomic stability. p53 activation is controlled by mechanisms involving post-translational modifications, protein interactions and modulation of subcellular localisation. Recently, p53 was identified within nuclear bodies, particular subnuclear structures that can provide a ‘platform’ where interaction of p53 with specific cofactors is favoured. Modulation of recruitment/release of some of these components and modifications might be required for directing p53 toward one or another of its downstream response pathways.