Interest in the mechanism of action of chloroquine is intense partly because of the emergence of drug-resistant parasites. Chloroquine resistance has been genetically linked to mutations in a parasite protein (PfCRT) that might confer resistance by inhibiting chloroquine accumulation in infected erythrocytes. Now chloroquine-binding proteins in malaria-infected erythrocytes, surprisingly, have been identified as human aldehyde dehydrogenase 1 and quinone reductase 2, raising the interesting possibility that the target of the anti-malarial activity of chloroquine might be a host enzyme.