During the course of evolution, all vertebrates have been exposed to multiple waves of cross-species infection by retroviruses. Some of these viruses have succeeded in infecting germ cells and are now inherited in integrated, proviral form (1). These so-called endogenous retroviruses have undergone further amplification and now make up a greater fraction of our DNA than do normal coding sequences (2). For a considerable while it was an open question whether these proviruses provided significant benefits to their hosts or simply represented junk or selfish DNA. It is now clear that several such elements contribute to protection against retroviral infection (3). Moreover, a number of lines of indirect evidence have pointed to a possible role in placental development (4). Now comes compelling evidence that one or more proviruses are “paying their way” with a specific contribution to normal physiology. In this issue of PNAS, Dupressoir et al. (5) show that mutant mice in which the syncytin-A gene has been knocked out die in utero, apparently as a result of the failure of trophoblast cells to fuse and form one of the two syncytiotrophoblast layers present in the placenta of mice. These structures are present on the exterior of the placenta, at the fetal–maternal interface, and are thought to play a key role in exchanging nutrients and waste between mother and fetus. Syncytin-A is derived from a retroviral env gene (6).