During kidney development, the formation of nephrons (the functional units of the kidney) involves the migration and condensation of nephron progenitor cells (NPCs). It has been shown previously that FGF8 regulates NPC survival but now, Florence Naillat, Dagmar Iber and colleagues report that FGF8 signalling plays a novel chemokinetic role in controlling NPC condensation in mice. The authors first show that, in the absence of Fgf8 expression, formation of the cap mesenchyme, which contains NPCs, is impaired and the attachment of cap mesenchyme cells to the ureteric bud is disrupted. They further demonstrate that, in 3D cultures in vitro, FGF8 induces the formation of NPC aggregates and promotes maintenance of a true (rather than a committed) NPC fate. Following on from this, the researchers use bead assays to show that FGF8 has mainly a chemokinetic effect on NPCs; computational modelling confirms this finding and suggests that the chemokinetic effects of FGF8 can indeed explain the distribution of NPCs. Finally, the authors report that late deletion of Fgf8 in mice leads to incorrect localization of NPCs within the nephrogenic niche. Overall, these findings suggest that FGF8 functions as an autocrine chemokinetic factor and coordinates the behaviour of NPCs during kidney development.