A retired but well-preserved mechanism for regulating viruses that has worked its way into the human genome appears to modulate a switch between adult and fetal hemoglobin production, researchers report. That switch could be the key to more targeted therapies for sickle cell patients whose misshaped adult hemoglobin hinders its ability to deliver oxygen throughout the body. Fetal hemoglobin, on the other hand, can't take on the dysfunctional sickle shape.