Two papers in this issue report that ZAG-1, the C. eleganshomologue of the vertebrate Zn-finger homeodomain protein δEF1, acts as a transcriptional repressor that regulates many crucial aspects of neuron terminal differentiation. Both groups discovered zag-1 in screens for mutant worms with defective neuronal development. These studies revealed that zag-1 mutations cause axon guidance, fasciculation and branching errors, and the misexpression of neuronal differentiation markers. The null mutant, as reported by Wacker et al. on p. 3795, also highlights the involvement of zag-1 in pharynx development as mutant larvae die from starvation, being unable to swallow food. On p. 3781, Clark and Chiu show that zag-1 is expressed in neurons and specific muscles,and directly represses its own expression, while also downregulating genes involved in neurotransmitter synthesis or reuptake. The authors expect future work on ZAG-1 targets to uncover novel and key regulators of axon guidance.