NLGN3 and autism: While one might fear that this progression toward faster and more defined neuronal induction will bypass normal neural development, potentially limiting the ability to observe early phenotypes such as neural migration, specification or maturation, we note recent evidence that iNeurons derived from patients with an autism-associated neuroligin-3 (NLGN3) mutation perfectly recapitulated the molecular and synaptic defects observed in the Nlgn3 mouse model (Chanda et al., 2013).