The inability to translate C/EBP α and β is associated with impaired hematopoiesis in SBDS, and more importantly, the 200-fold elevated risk of developing AML in SDS patients,225 as loss-of-function mutations in C/EBPα have a known role in AML pathogenesis.226 The current findings support the hypothesis that altered translational capacity and fidelity resulting from defective ribosomes contribute to cancer development by facilitating the production of oncoproteins and/or activation of oncogenic pathways. This evidence concerns the gene CEBPA and acute myeloid leukemia.