In line with these findings, Rahman et al. showed that (i) exogenous administration of IL-1β in heterozygous JAK2V617F knock-in mice, that mainly exhibit a PV-like disease phenotype, fostered disease progression (granulocyte and megakaryocyte hyperplasia coupled with impaired erythropoiesis, and increased reticulin fibers); (ii) IL-1R1 blockade by anti-IL1R1 antibodies was capable of significantly reducing the disease stigmata in a homozygous JAK2V617F knock-in mouse model of MF (normalized blood cell counts, reduced spleen size, BM fibrosis, and abnormal MK clustering) [15]. The gene discussed is IL1R1; the disease is fibrosis.