[5] In vitro colony forming assays with bone marrow cells from patients with DBA demonstrated a decreased proliferation and increased apoptosis in erythroid colonies that pinpoints the defect to the erythropoietin-dependent stages of RBC differentiation. [6], [7], [8] Additionally, in vitro culture studies and studies in animal models of DBA demonstrated that inactivation of p53 improves or even restores RBC production, suggesting a p53 dependent cell cycle checkpoint may be involved in pathogenesis [9], [10]. The gene discussed is EPO; the disease is Diamond-Blackfan anemia.