JAK2 V617F clonal disorders: Fate or chance?

Abstract

In this issue of Blood, Hinds et al identify several novel polymorphic genomic loci that are associated with an increased risk of developing JAK2 V617F-driven clonal hematopoiesis and myeloproliferative neoplasms (MPNs).1 Their findings affirm the notion that, although the acquisition of somatic mutations in hematopoietic stem cell (HSC) genomes is an infrequent and apparently stochastic process, the fate of mutant cells and their clonal progeny is profoundly influenced by heritable genetic polymorphisms present in the host's genome.