Given the previously described role of HSP27 in the proteasomal processing of GATA-1, HSP70, and HSP27 thus cooperate in the fine-tuning of terminal erythropoiesis through the regulation of GATA-1 content and activity.15 Confirming the essential role of HSPs in erythropoiesis, defaults in HSP post-translational modifications and/or in their subcellular localization lead to red blood cell pathologies, as evidenced in myelodysplastic syndromes (MDSs)19 and in beta-thalassemia major (β-TM).20 The gene discussed is GATA1; the disease is beta-thalassemia major.