Abstract
Wendt and Collins identify a cyclin-dependent kinase inhibitor (cki) in Schistosoma mansoni that, along with p53-1 (schistosome homolog of TP-53), suppresses tegument cell proliferation. Knockdown of cki causes hyperproliferation and, together with p53-1 loss, tumorlike growths. Homologs of cki are widespread in parasitic flatworms but absent in free-living relatives, suggesting that the horizontal gene transfer aided the evolution of parasitism.