According to the `clock and wavefront' model of somitogenesis, a segmentation clock driven by oscillations of Notch, Fgf and Wnt signalling in the presomitic mesoderm (PSM) is translated into a periodic array of somites at the so-called wavefront. Wnt3a/β-catenin signalling is widely believed to be a component of this clock, but on p. 85, Terry Yamaguchi and colleagues surprisingly suggest otherwise. To study Wnt3a's role in somite segmentation, the researchers introduced conditional loss- and gain-of-function β-catenin alleles into mice. Their findings show that although Wnt3a is necessary for the clock gene oscillations that occur during somitogenesis, Wnt3a/β-catenin signalling does not function as an integral component of the segmentation clock because small, irregular and abnormally located somites do develop in the absence of β-catenin and cycling clock gene expression. From their results, the researchers conclude that Wnt3a/β-catenin signalling has a permissive, rather than an instructive, role in the oscillation of clock genes, and that it controls somite boundary formation by regulating the anteroposterior position of segment boundary-determining genes.