Louis H. Miller sion of the infection. There must be some block to the development of the parasite in Culicine mosquitoes that the human parasite is unable to overcome. Introduction of genes encoding refractoriness into field populations of mosquitoes remains a major obstacle to implementation of such control strategies. A transposable element, the P element, first appeared in Drosophila melanogaster around 1950 and spread in a non-Mendelian fashion to flies of this species around the world (9). We might use an analogous transposable element of mosquitoes in a cassette with genes for refractoriness to malaria to introduce these genes into vector populations. The third leg of basic research aimed at developing new tools is the identification of biochemical pathways unique to the malaria parasite and subsequent development of poisons specific to the parasite. One such area is hemoglobin digestion. The parasite, after digestion of hemoglo-bin, reorganizes heme into a nontoxic compound, hemozoin pigment. The polymeric structure of hemozoin pigment has recently been identified, and the polymerizing enzyme activity is blocked by chloroquine and other related antimalarial compounds (10). Furthermore, the locus for the chloroquine resistance gene (11), which encodes a drug-efflux mechanism (12) unrelated to the polymerase, has been identified. Understanding the structure and function of the polymerase and efflux mechanism should open the way for drug design to reverse chloroquine resistance. Malaria, unlike AIDS, is not a major health problem for citizens of the United States; it is a problem of the unseen sick and dying in the villages of the tropical world. Our goal must be to develop tools and ways of delivering these tools to limit disease and to prevent malaria at a costthat is affordable and sustainable in these populations with limited resources. Success will demand continual support of basic scientists and involvement of industry. Can we ignore this challenge?