Ischemic stroke is a neurological condition characterized by loss of blood flow in the brain due to blood clots. Epigenetics is a relatively new field of biology that centers around the factors that regulate gene expression without actually changing the genetic code itself. One example of an epigenetic modulation that occurs to DNA after a stressful event like stroke is methylation of the fifth carbon on the cytosine of DNA. This 5-methylcytosine has been experimentally shown to inhibit gene expression and lead to poorer outcomes after stroke. Ten-eleven translocase proteins (TETs) are responsible for converting that methyl group into a hydroxymethyl group. Though this pathway is not well-understood, it is clear that the conversion of 5-methylcytosine to 5-hydroxymethylcytosine plays a neuroprotective role after stroke. Thus, by either pharmacologically activating or inhibiting TET enzymes and then simulating a stroke on the cells, we could see whether the relative amount of 5mc or 5hmc lead to a difference in cell death. We were able to show that pharmacologically activating TETs lead to less cell death and inhibiting TETs lead to more cell death. This provided a promising background for how TETs are able to regulate faster recovery post-stroke.