More detailed investigations of RE silencing/de-silencing mechanisms in normal and disease states are warranted in view of the key role of RE in homeostatic control of tissue function and the fact that repeat element activation in cancer cells induces chromatin reprogramming and chronic inflammatory signaling via interferon and NFκB which together are responsible for tissue microenvironment remodeling (immune and stromal cells) downstream of the viral mimicry response [3]. The gene discussed is NFKB1; the disease is cancer.