The bone marrow as the site of thrombopoiesis becomes both exhausted and suppressed as part of the dysregulated host response in sepsis.22 Septic neonates produce an excess of thrombopoietin (TPO), and the eventual development of thrombocytopenia may represent an “exhaustion” of marrow resident megakaryocytes and their precursors rather than a depression.23,24 This is particularly important as the neonatal megakaryocyte precursors, while responsive to TPO, tend to increase in number but not in size in response to stimulation. This evidence concerns the gene TPO and Thrombocytopenia.