In MPN, preclinical data strongly supports the effect of HDACi inhibiting proliferation and inducing apoptosis in JAK2 mutated cells, normalizing splenomegaly and blood counts in JAK2 mutant knock-in mice [53] and promoting proteasome mediated JAK2 degradation by disrupting HSP90 chaperone function. Here, JAK2 is linked to myeloproliferative neoplasm.