Our DNA exists in threadlike structures, called chromosomes, that contain protective caps, called telomeres. The telomeres prevent underlying important chromosomal DNA from being eroded, much like shoelaces’ caps prevent the delicate underlying fabric from becoming unraveled. When most cells grow and split into two new “daughter” cells, their telomeres get shorter. Over time, as cells repeatedly divide, the telomeres progressively shorten until a critical length triggers cell death. This is a natural process that removes “old” cells from the body. However, in 80-90% of human cancers, an enzyme is pathologically active that lengthens the telomeres, effectively making cancer cells “immortal.” It is unclear how telomerase becomes reactivated in cancer. Of particular interest is regulation of the telomerase reverse transcriptase gene (TERT), which is the active subunit of the telomerase enzyme, and is required for telomerase activity. Cancers with only one active copy of TERT have been found in the majority of cancerous tissue types. In some of these, the active copy contains no DNA mutations responsible for reactivation. We discovered molecular (i.e., epigenetic) patterns associated with the active TERT copy that may help with better understanding its reactivation. This could eventually help guide future drug discovery and cancer therapeutic efforts.