The abundance and variety of TEs within mammalian genome and their well-documented co-opted functions implies that these elements have, in part, driven the evolution of host genomes. However, a complete picture of the mechanisms governing this co-evolution as well as an understanding of the extent to which our genomes have been shaped by TEs is lacking. A major hurdle in comprehensively charting the co-evolution of host genomes with these friendly foe lies in the expanse of past and future evolutionary time that we cannot see. While ancient transposons which may have shaped the genomes of our ancestors are now decayed, often beyond recognition, the youngest, full length TEs are still active which means that, posing a threat to genome integrity, they must be silenced by the host. It is likely that these then remain far from being co-opted. To address this, we have established a model of transposon-host genome evolution in human stem cells; by introducing a novel transposable element to human cells – a young and active mouse TE IAPEz element – we are modelling TE invasion, fixation, regulation and co-option. Utilising comparative epigenomics, single cell locus specific TE-sequencing and single cell transcriptomics we are exploring the potential for host cells to use TEs to adapt under selective pressure and comprehensively cataloguing the genetic and epigenetic mechanisms via which this occurs. Our data suggests that over an adaptive time-course cells may utilise novel or “unannotated” enhancer regions which are enriched for LTR-transposons, implicating these TEs as being poised for their consequent co-option as cis-regulatory elements under the need to adapt to external stress.