Subsequently, we plan to validate our mechanistic findings in further studies, utilizing primary MPN patient samples harboring BRCA1 mutations and haploinsufficient Brca1 animal models to assess how the concept of synthetic lethality between BRCA1 haploinsufficiency and PARP inhibition translates clinically into JAK2V617F-driven MPN. This evidence concerns the gene BRCA1 and myeloproliferative disorder.