When erythropoietin won market approval in 1988, it was hailed as a wonder drug because of the selectivity of its action and its resulting relative freedom from untoward effects. This selective action was due largely to the restricted expression of its receptor on erythroid progenitors. As is common with “wonder” drugs, however, things turned out not to be quite so simple. Over the ensuing years, functional erythropoietin receptors have been shown to be present on other types of cells, but these findings have had little effect on the therapeutic uses of erythropoietin — although some of them could be advantageous . . .