Interestingly, RPS24-deficient cells showed increased levels of the cell cycle inhibitor p21 and a seemingly opposing increase in Cyclin-E, CDK4 and CDK6. The exact mechanism of DBA may be a combined effect of ribosome synthesis and p53 activation, and more efforts are needed to correlate specific mutations to the disease phenotypes such as its impact on erythropoiesis. This evidence concerns the gene TP53 and Diamond-Blackfan anemia.