However, many cancers have innate or acquired resistance to nucleoside analogues, markedly limiting their efficacy.1–5 For gemcitabine, expression of proteins required for transport, activation and/or breakdown of the drug has been correlated with treatment resistance and adverse survival outcome.6,7 The transport of gemcitabine into cancer cells is mainly mediated via human equilibrative nucleoside transporter 1 (hENT1). The gene discussed is SLC29A1; the disease is cancer.