To validate the connection between RUNX1 expression and fibrosis in the dysregulated niche in MPN, we first asked the question of whether the JAK2V617F mutation leads to the increased expression of Runx1. HoxB8 cells transduced with the JAK2V617F mutation demonstrated a significant increase in Runx1 expression compared to the cells expressing wild-type JAK2 as a control, indicating that the increase in Runx1 expression is driven by the MPN clone (Figures S2C and S2D). This evidence concerns the gene JAK2 and myeloproliferative disorder.