Using astroglial cultures from mouse models of Rett syndrome, the Human Neurogenetics team has identified by mass spectrometry deregulated proteins that cascade into abnormal neuronal function. Two of these proteins, Lipocalin2 and Galectin3, when added to cultured neurons, correct the reduced neuronal arborization seen in the pathology. These results, published in the International Journal of Molecular Science, confirm the fact that Rett syndrome is both a neuronal pathology and that good neuron/glia exchanges are necessary to prevent its development.