All showed pronounced BM aplasia and strong expression of both proteins across most hematopoietic cells – markedly higher than in an age-matched healthy control and a pediatric patient with severe aplastic anemia (Fig. 7; Supplementary Fig. 11), suggesting a conserved role of the p53/PUMA axis in TBD pathogenesis. This evidence concerns the gene BBC3 and idiopathic aplastic anemia.