In addition, MPN-related driver mutations, including JAK2 V617F, exert broad pro-inflammatory effects and contribute to maintenance of the malignant inflammatory microenvironment, as well as evasion from T cell immunosurveillance, eventually resulting in uncontrolled clonal escape, providing a potential opportunity for development of B cell tumors (9). This evidence concerns the gene JAK2 and myeloproliferative disorder.