Despite differing hallmark oncogenes we have shown a degree of similarity between the proteomic perturbations observed in CML and PV and that dual targeting of p53 and MYC is successful in eradicating the leukemic stem cell in both BCR/ABL and JAK2 associated MPNs.11,12 Here, we describe another such outcome from our proteomic screens and demonstrate that inhibition of AXL represents a novel therapeutic approach in JAK2 induced MPNs suitable for evaluation in clinical trials. The gene discussed is JAK2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.