RNA editing enzymes have been known for some time to affect the qualitative and quantitative nature of RNA products. RNA editing has also been correlatively linked to the mediation of behaviour of organisms ranging from flies to humans, with the highest levels of these enzymes in humans. Mechanistically, this has been suggested to occur by their ability to bind to RNA and participate in deamination of: cytosine in the case of APOBECs’, or adenosine in the case of ADARs’. However, two caveats arise in the proposed relationship. One is that not all variants of these enzymes appear to operate solely by this mechanism; they can also bind to DNA. And two, that much of the mechanistic work for this latter point has been divorced from a behaviourlly relevant context. Therefore, in order to assess the function of these domains in the context of behavioural adaptation, genome-wide DNA sequencing for ADAR1 was performed both with cultured primary cortical neurons (PCN’s) and 6-8 week old C57 mice subjected to fear conditioning and extinction. An shRNA was also designed against ADAR1 and transfected with PCN’s and into the infralimbic cortex of the trained mice. It has been observed that ADAR1 appears to bind a number of targets on DNA. Additionally and surprisingly, it was observed that although mRNA and protein levels appeared elevated specifically to extinction behaviour, following knockdown of ADAR1 in the infralimbic cortex the expression of fear was enhanced, while fear extinction remained unaffected. It remains to be seen whether this effect is mediated primarily by ADAR1’s RNA editing activity or the binding capacity to DNA.