The landscape of genetic alterations in B-ALL was extended by the identification of loss-of-function mutations (either deletions or sequence mutations) of CREBBP, encoding the transcriptional coactivator and histone acetyltransferase CREB-binding protein or CBP, in 19 % of relapsed samples from children with B-cell progenitor ALL [54•]. This evidence concerns the gene CREBBP and acute lymphoblastic leukemia.