It appears that this cellular safeguard system may also have been repurposed by the host in order to aid in transient defenses against invading viruses: infection-triggered loss of SUMOylated TRIM28 (a putative ‘SUMO-switch’) leads to derepression of immunostimulatory ERVs and the potentiation of IFN-mediated immunity [36] (Figure 6). The gene discussed is IFNA1; the disease is infection.