Valproic acid (VPA) is widely used to treat epilepsy, bipolar disorders and migraines. Its anticonvulsant activities were discovered by chance in 1963, and it was approved as a drug in 1967. More than 40 years later, it was still unclear how this chemical enters cells, but Robin Williams and colleagues (p. 2267) now describe an uptake mechanism for VPA. They find that in Dictyostelium discoideum the short-chain aliphatic acid becomes enriched in the cytoplasm, without being covalently bound to proteins or other lipids, and that VPA uptake is pH-sensitive and dependent on a proton gradient. Making use of the fact that VPA blocks growth and retards development in this social amoeba, the researchers identify a VPA-resistant Dictyostelium mutant in a genetic screen. The phenotype is caused by a disruption in the gene encoding a membrane protein that is homologous to the mammalian solute carrier family 4 (SLC4) bicarbonate transporter. The authors show not only that SLC4 is involved in VPA uptake in Dictyostelium, but also provide evidence that this mechanism is conserved in zebrafish and Xenopus laevis, and that blocking this transporter prevents the teratogenic side-effects of VPA. They hope that the identification of SLC4 as a mediator of active VPA transport into the cell will enable better regulation of drug uptake into target tissues and reduce side-effects of this anticonvulsant drug in the future.