These results are consistent with those reported for hematopoietic cells, in which the kinase domain of Jak2 inhibits cell death and treatment with the Jak2 inhibitor AG-490 reduces phosphorylation of PI 3-kinase, resulting in increased caspase 3 activity and Bax protein in acute myocardial infarction [31]. Here, JAK2 is linked to acute myocardial infarction.