The membrane transport of cytosine arabinoside (araC) has been studied in blasts freshly isolated from a variety of acute leukaemias. The major fraction of araC influx was facilitated and this fraction was 80-87% at l microM araC and 68-80% at 200 microM araC. Competitive kinetics were observed between araC and deoxycytidine for entry into leukaemic blasts and, moreover, araC influx was blocked by phloretin, a broad-spectrum inhibitor of facilitated transport systems. Kinetic analysis of facilitated araC influx gave KmS which varied over a 10-fold range between patients and which were positively correlated to the Vmax. Nucleoside influx Vmax also varied over an 80-fold range between individuals, although the mean araC transport was 4-fold greater in myeloblasts than in lymphoblasts. Larger transport of araC may explain the greater sensitivity of acute myeloid leukaemia to this drug.