Ever since I can remember, I've been fascinated by the fact that a major proportion of our DNA is actually of viral origin - known to the scientific community as the human endogenous retroviruses (ERVs). Surprisingly, ERVs comprise over 8% of our DNA, whereas only 1% of our DNA actually codes for our own proteins. On top of that, these retroviral-derived sequences govern the very nature of our existence! Placental mammals, including humans, may not have come into existence without the aid of the ancient retroviruses. This is because human genes that encode for proteins crucial for placental formation are derived from an ERV. In addition to providing such biological benefits to their human hosts, some ERVs have also been speculated to be associated with a variety of diseases, ranging from neuro-degeneration and rheumatic disease to multiple types of cancers. Although majority of ERVs have been silenced through accumulation of mutations over evolutionary time, some belonging to the ERVK group have been shown to be re-activated under inflammatory conditions. Unfortunately, we do not yet understand the mechanism(s) behind their re-activation. Thus, a major focus of my research is to determine which human cellular proteins induce ERVK in our cells during inflammation. In addition, my motivation for choosing this research path stems from the fact that I have a long family history of ERVK-associated diseases, particularly arthritis and lupus. Overall, this research is worthy of recognition and support because of its novelty and importance in understanding the pathogenic processes behind ERVK-associated diseases.