Our data indicate that selective disruption of IL-1 signaling in the BM microenvironment attenuates Jak2V617F-induced BM fibrosis without affecting hematopoietic phenotypes, whereas hematopoietic disruption of IL-1 signaling reduces both MPN hematopoietic phenotypes and BM fibrosis. The gene discussed is IL1B; the disease is myeloproliferative neoplasm.