These data, of course, should lead us to search for a broader explanation of the mechanisms by which the JAK2 46/1 haplotype predisposes to MPN, which likely goes beyond the “hypermutability” or “fertile ground” hypotheses, which can explain the association with JAK2V617-positive but not with JAK2V617F-negative cases (i.e., increased mutation rate of the JAK2 locus and selective advantage of the JAK2V617F mutated clone) [18]. This evidence concerns the gene JAK2 and myeloproliferative neoplasm.