In order to address the role of IL-1 signaling in BM microenvironment and its contribution in the pathogenesis of Jak2V617F-induced myelofibrosis, we crossed IL-1R1 floxed mice26 with Prx1Cre transgenic mice32 to generate Prx1Cre; IL-1R1F/F mice that allow Cre-mediated deletion of IL-1R1 in BM mesenchymal stromal cells (MSC). This evidence concerns the gene IL1A and myelofibrosis.