Published studies confirmed that ruxolitinib caused DNA repair defects and sensitized MPNs stem and progenitor cells to poly-ADP-ribose polymerase (PARP) inhibitors olaparib and BMN673, and HU induced DNA damage; therefore, ruxolitinib and olaparib plus or minus HU were very effective in vivo against JAK2 (V617F)+ murine MPN–like disease (30). The gene discussed is JAK2; the disease is myeloproliferative disorder.