These mice showed a dramatic decrease in progenitor cells and a delayed erythroid differentiation without obvious myeloid and lymphoid lineages defects (Fig 5), a phenotype reminiscent to the defect described in CD34+ cells from DBA patients with inherited RPL11 mutations, underlining the importance of the co-ordination of ribosome biogenesis with cell cycle control in erythropoiesis[30]. This evidence concerns the gene CD34 and Diamond-Blackfan anemia.