Much of our DNA is repetitive sequence comprised of mobile genetic elements. Cell's energy expenditures associated with their life cycle and containment are negligible in normal conditions, as human cells have evolved to coexist with transposable elements and use them to their advantage. In disease, when genome defense mechanisms are compromised, energy costs associated with transcription, translation and integration of mobile elements soar. Here we demonstrate how a competition between two major types of human transposons may determine cell fate in pathological conditions.