JAK2 transmits intracellular signals downstream of cytokine receptors as it phosphorylates and activates STAT [132] and regulates TET2 in response to cytokines, thereby linking extracellular signals with epigenetic modifications in hematopoiesis [133] The JAK2 V617 F gain-of-function mutation, commonly associated with myeloproliferative neoplasms (MPNs), significantly increases the risk of thrombotic events, myocardial infarction, deep vein thrombosis, and stroke [134]. Here, JAK2 is linked to myocardial infarction.