Autism Spectrum Disorder and Obsessive Compulsive Disorder are comorbid disorders that share a neurodevelopmental origin. They present themselves most notably through abnormal behavior, but recent studies have looked into their genetic and epigenetic markings. This summer project aimed to look at the epigenetic role of the Mll3 gene in autistic behavior in mice. Using an openfield setup along with a behavior analysis pipeline that I had created, we ran and analyzed wild type and heterozygous knockout mice and quantitatively analyzed their behaviors. We found that mice heterozougous for the gene displayed more exploratory behavior and less anxiousness along with less grooming of themselves. These results do suggest the importance of the Mll3 gene in studying autism. We then looked at the Nrxn1 gene, famously studied for understanding more about autistic behavior. However, with the help of another lab, we studied the recovery of the Nrxn1 gene in mice with it originally knocked out. We found no significant difference between the WT mice and recovery mice in terms of locomotion or behavior. However, the knockout mice also didn’t show any reduced or increased behavior types along with locomotion, so we have since run more animals to try and increase the power of the study and potentially find some difference. If we do observe some, that would indicate normal behaviors can be recovered from the autistic phenotype through gene manipulation, an extremely important point for clinical relevance. Lastly, we looked at the Slitrk5 gene, previously known to play a role in obsessive compulsive disorder behavior. In the same experiment setup as the Mll3 gene, we ran 5 WT and 5 KO mice. However, we found no significant difference in locomotion or any repetitive behaviors, but this could be a result of such little amount of mice used so far.