Upon investigating H3K9me3 at the CCL3 gene of sex dimorphic EPCs, we found high H3K9me3 occupancy at the TSS in F-EPC and OVX EPC and no methylation in the TSS of the M-EPC contributing to enhanced secretion of CCL3 by M-EPC resulting in augmented pathogenesis when injected in post-MI mice. Here, CCL3 is linked to myocardial infarction.