At the cellular level, Arxbound promoters are enriched for genes important for nuclear transport, cell adhesion or migration, RNA processing, cell fate commitment and regulation of multicellular process through the regulation of several important signaling pathways including Gprotein coupled-receptor, adenylate cyclase activity or neuroactive ligand-receptor interaction . Interestingly, several genes identified in N2a-transfected cells and embryonic brain were associated with axonal guidance and long-term depression and/or long-term potentiation, suggesting a possible function of Arx in synaptic plasticity . We also examined in more detail Arx targets associated with neuronal function. As shown in Table 1, a certain number of them have been associated with dyskinesia and neurological disorders including phenotypes observed in ARX-mutated patients. Using publicly available in situ hybridization data in mouse , we next investigated the expression of some Arx candidate target genes . In the developing cortex, Arx has been shown to be expressed in progenitors of the dorsal ventricular and subventricular zones as well as in tangentially migrating inter204005-46-9 neurons coming from the ganglionic eminences but not in radially migrating cells. On the contrary, in the basal telencephalon, Arx is strongly expressed in differentiated neurons but not in proliferating cells of the lateral and medial ganglionic eminences . As shown in Figure S1, several ChIP-positive genes are expressed in the developing telencephalon at E14.5, either in the cortical ventricular zone, or in regions containing migrating and/or differentiating interneurons. For example, at E14.5, Epha3, Sema3c, Cxcr7 and Snrpn appear to be expressed in cortical migrating neurons, whereas Bhlhb5 and Gabrb3 seem to be restricted to differentiating neurons in the cortical plate. Genes such as Cdh2, Rpn1, Nxf1 and Tle1 appear to be also expressed in cortical neuronal progenitors. Finally, genes like Tle1, Hist1h4h, Hist2h3c, Rpn1 and Nxf1 also localize to developing ganglionic eminences suggesting a possible role in interneuron development . As binding does not necessarily imply regulation, we next checked whether the putative targets identified by ChIP-chip were differently regulated following Arx overexpression.