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Myeloproliferative neoplasms (MPNs) are a series of blood disorders that tend to lead to acute myeloid leukemia (AML). The most common genetic mutation in MPNs is called JAK2V617F, an activating mutation in JAK2 kinase. Although JAK2V617F has been associated with increased DNA damage, MPNs are diseases characterized by genomic stability.

In a recent paper published by , ӳý associate member and senior author Ann Mullally, first author Edwin Chen, and colleagues address this paradox by showing that a DNA helicase called RECQL5 suppresses genomic instability in MPNs even as JAK2V617F instigates a state of DNA damage.

In the years since the human genome was first sequenced, a trove of genomic data has been amassed, aiding not only in our understanding of how the body works, but also in the search for disease-fighting drugs. Indeed, finding connections between idiosyncrasies within the genome and effective treatments is the hallmark of “precision medicine,” a growing movement that aims to target therapeutics to those who would most likely benefit from their use.