Contact inhibition of locomotion (CIL) is a fundamental regulatory mechanism that ensures correct cell movement and migration. During CIL, cells form transient contacts but the molecular nature of such contacts is unknown. In this issue, Roberto Mayor and colleagues (p. 4763) investigate the role of the cell polarity protein Par3 in microtubule collapse and reorganisation during CIL in migrating neural crest cells. Using antisense morpholinos to Par3 in Xenopus and zebrafish, the authors show that loss of Par3 has a dramatic effect on migration and is essential for CIL both in vitro and in vivo. Par3 knockdowns fail to exhibit microtubule collapse at the cell-cell contact; however, this can be rescued by injection of an antisense morpholino to Trio, implicating the Rac-GEF Trio in migrating neural crest CIL. The authors propose a model in which CIL requires the local destabilisation of microtubules at the cell-cell contacts, which is controlled in a Par3/Trio-dependent manner.