The occurrence of these lymphoproliferative disorders was preceded by the accumulation of lymphoid progenitors characterized by a hyperproliferative state and an altered DNA damage response linked to the loss of p53 activation in the absence of Crebbp. Interestingly, the authors found no enrichment for Bcl6 targets among Crebbp binding sites in their system suggesting different epigenetic changes when Crebbp is deleted in hematopoietic stem cells (HSC). Here, CREBBP is linked to lymphoproliferative syndrome.