INTERFERONS constitute a class of biologically active glycoproteins1-3 which induce a spectrum of physiological changes in living cells, leading to the inhibition of virus replication4, of cell growth in vitro-both normal and tumour cells5,8-and of tumour growth in vivo9-15. The mechanism(s) underlying these effects is unknown. Gressor et al. have suggested that the same molecule in an interferon preparation is responsible for both the antiviral (AV) and cell growth inhibitory (CGI) effect5. This suggestion was based on the observation of a consistent and direct correlation between the two effects in an interferon preparation purified more than a millionfold. Gressor also reported that tumour cells treated with interferon had a lower capacity to form colonies in Agarose and were less tumorigenic when innoculated15, suggesting that the antitumour effect of interferon depended, in part, on the inhibition of tumour cell multiplication which can be demonstrated in vivo. I describe here a genetic approach to ascertain whether the CGI effect of human interferon preparations is mediated by chromosome 21-directed gene(s), known to govern the AV action of interferon16-19. Such an approach, should provide further insight into whether the different effects of interferon are governed by a cluster of genes on chromosome 21 or whether a single genetic locus on chromosome 21 codes for the pleiotropic effects of interferon.