A tumour-suppressor role for these global HATs has been strongly suggested from many sources: CBP, p300 and pCAF somatic mutations have been described in primary human tumours (Gayther et al, 2000; Ozdag et al, 2002; Ionov et al, 2004; Kishimoto et al, 2005); patients with Rubinstein–Taybi syndrome, caused by germline mutations in the CBP gene, have an increased tendency to develop tumours at an early age (Gibbons, 2005); and CBP heterozygous mice develop haematological tumours (Gibbons, 2005). Here, EP300 is linked to neoplasm.