These models also support the hypothesis that there is a causal link between altered signaling at α subunits of the GABAA receptor and the emergence of schizophrenia-relevant dysfunctions in neurodevelopmentally compromised offspring (Stan and Lewis, 2012; Volk and Lewis, 2013), at least with respect to AMPH hypersensitivity and related hyperdopaminergic functions. This evidence concerns the gene AMPH and schizophrenia.