Targeted integration of exogenous DNA into the genome of malaria parasites will allow their phenotype to be modulated by means of gene disruption or the stable expression of foreign and mutated genes. Described here is the site-specific integration through reciprocal exchange, and subsequent expression, of a selectable marker gene into the genome of the pathogenic, bloodstage forms of the rodent malaria parasite Plasmodium berghei. Stable integration of a single copy of the marker gene (retained for more than 70 generations in the absence of drug pressure) into a nontranscribed subtelomeric repeat array of different chromosomes was observed. Expression of the gene within the subtelomeres indicated that the previously recorded absence of transcription in these regions could be due to a corresponding absence of genes rather than active silencing mechanisms.