The excessive TNF-α cause various profound effect on the milieu of MPN: platelet hyperreactivity and mitochondrial dysfunction (17); venous thromboembolism risk (18); accelerate fibrocyte production and reticulin fibrosis deposition in ASXL1-mutated patients (19); favors the JAK2V617F mutated cells in survival and clonal expansion over unmutated cells (20, 21). The gene discussed is TNF; the disease is venous thromboembolism.