A lethal contagious disease, Devil Facial Tumour Disease (DFTD) is ravaging the population of Tasmanian devils, Sarcophilus harrisii. The cells of this cancerous disease themselves act as the infectious agent, and are spread through the devil’s social biting interactions. Although the devil’s immune systems should reject these foreign infectious cancer cells through processes such as cell self-recognition by MHC detection, DFTD has evolved to evade such immune responses and is able to freely infect devils. This is believed to be, in part, driven by aberrant epigenetic changes within DFTD cells. Given its ability to propagate, DFTD is able to, and has been, evolving since its emergence last century. One such feature of its evolution is its ongoing DNA demethylation. However, it is not known if these demethylation changes occur globally across the genome or are more locally targeted; this could have varying implications for the evolution of DFTD and the stability of the cell line. Using immunostaining and immunofluorescence microscopy, in tandem with gene mapping techniques, this project will examine what regions of the genome are targeted by DNA demethylation, and will further extend this study to various other epigenetic markers, such as certain histone modifications, to identify ongoing epigenetic changes within DFTD cells and whether they are globally or locally targeted.