In zebrafish acerebellar (ace) embryos, a point mutation in fgf8 prevents the formation of the isthmic constriction, which contains the midbrain-hindbrain boundary organiser, leading to the loss of cerebellar development and the formation of an enlarged tectum. On p. 6611,Jászai et al. report that these morphological features are the result of an alteration of cell fate in the fgf8 mutant brains. By comparing gene expression patterns in wild-type zebrafish and ace mutants, the researchers demonstrate that a caudal-to-rostral switch in cell fate underlies the tectal expansion in the mutants and that this transformation is not due to alterations in cell proliferation or cell death. They also report that implantation of Fgf8-coated beads into the prospective midbrain-hindbrain boundary rescues the ace mutant phenotype, indicating that the absence of the inductive organiser signal Fgf8 is responsible for the cell-fate alterations seen in the ace mutant.