Indeed, in previous studies from our group, we found that megakaryopoiesis was enhanced in PKCδ null mice and PKCδ null mice recovered faster from an immune-mediated thrombocytopenia as compared to wild type mice[50], suggesting that PKCδ is an important regulator of platelet formation and PKCδ inhibition could also increase megakaryopoiesis during sepsis. This evidence concerns the gene PRKCD and Sepsis.