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Anti-Inflammatory Effects: ACE inhibitors reduce levels of pro-inflammatory cytokines such as IL-6 and TNF- α while inhibiting NF- κ B activation, a critical mediator of inflammation in MPNs ( Anti-Fibrotic Properties: These medications suppress TGF- β signaling, a primary driver of bone marrow fibrosis ( Cardiovascular Protection: ACE inhibitors enhance endothelial function ( 2.1.3 Clinical and preclinical evidence in MPNs In PV: Treating PV patients with ACE inhibitors has been shown to be associated with a reduced need for cytoreductive medications ( Thrombotic Risk Reduction: In a large cohort of ET and PV patients with hypertension, the use of RAS inhibitors was associated with a significant reduction in thrombotic events ( In MF: In mouse models of MF, the ACE inhibitor captopril reduced both spleen size and the degree of bone marrow fibrosis ( Kidney Function: ACE inhibitor use was associated with improved estimated glomerular filtration rates (eGFR) in PV patients ( Symptom Burden: It is important to note, however, that ACE inhibitor therapy was not associated with an improvement in the systemic MPN symptom burden ( 2.1.4 Broad impacts of ACE inhibitors While the cardiovascular benefits of RAS inhibition are well-established, a meta-analysis of 158,998 patients notably found that ACE inhibitors—but not ARBs—were associated with a significant 10% reduction in all-cause mortality ( 2.2 Controlling lipids (statin) Dyslipidemia is the second most common cardiovascular risk factor in MPNs after hypertension ( 2.2.1 Mechanistic rationale in MPNs The primary pharmacological action of statins is the inhibition of HMG-CoA reductase ( More compellingly, a direct, disease-specific mechanism has been identified