TP53 and bone marrow failure syndrome: In DC and the related inherited bone-marrow failure syndrome Fanconi anaemia, loss of the hematopoietic stem cell niche is accompanied by activation of the p53/p21 axis, inducing a replicative senescent phenotype.45, 46, 47 Furthermore, studies on transgenic mouse models of nucleotide deficiency reported that the fine-tuning of nucleotide metabolism pathways is required for resolution of replication stress and overcoming maturation defects of hematopoietic stem and progenitor cells in vivo.48