In this study, the authors show that the absence of hematopoietic CXCL4 ameliorates the MPN phenotype, reduces stromal cell activation and BM fibrosis, which in turn decreases the activation of profibrotic pathways in Mks, inflammation in fibrosis-driving cells, and JAK activation in both Mks and stromal cells in three murine PMF models (TPOhigh, JAK2V617F, MPLW515L). The gene discussed is PF4; the disease is myeloproliferative disorder.