These two genes are involved in human cancers, particularly breast and ovarian cancers, and show increased expression in cancerous cells. Then, by fusing the transactivator protein VP64, they were able to dramatically increase the transcription of the genes. This condition can lead to clotting, vascular damage, thrombosis, and extensive tissue and bone damage in adults.
All humans have a redundant hemoglobin gene, however.
The fetal hemoglobin gene is always normal in adults with the sickle cell mutation, and as a result, people do not suffer from sickle-cell anemia as infants. At some point in early development, though, the responsibility for producing the body's hemoglobin switches from the fetal gene to the adult gene. A number of drugs already exist that increase the ratio of fetal to adult hemoglobin in the body, but they are all rather toxic. This sort of therapy would seek to insert the gene for the zinc finger regulatory protein into stem cells of a patient suffering from sickle-cell anemia. Then these stem cells would grow into red blood cells that would express the normal, fetal hemoglobin.