However, extension of this interpretation to human cells or other chromosomal environments is clouded by the observations that, in contrast to the transgenes, both upstream and downstream origins were equally active in human control and DM1 fibroblasts, while integration of the nonexpanded control (DM20) DMPK locus resulted in inactivation of both upstream and downstream origins in the transgenic mice. The gene discussed is DMPK; the disease is myotonic dystrophy type 1.