Using combinations of control and Rett Syndrome-derived astrocytes and interneurons, the authors show that the glial effect on neuronal function is independent of intrinsic deficits in neurons themselves and demonstrated that insulin-like growth factor (IGF-1) and GPE (a short peptide containing the first 3 amino acids of IGF-1) are capable of partially rescuing the astrocyte-mediated neuronal phenotypes. The gene discussed is IGF1; the disease is atypical Rett syndrome.