We have presented preliminary evidence that the neurodevelopmental transcriptional regulator PAX6 interacts with HOMER3, DNCL1 and TRIM11. We suggest that the interaction of PAX6 with HOMER3 and DNCL1 is a mechanism by which synaptic signalling could lead to regulated changes in gene expression in neurons. We also propose that some of the neural anomalies in patients with PAX6 mutations may be explained by impaired protein-protein interactions.