The robust deficit in social interaction and the heightened anxiety of Nrxn2α KO mice are consistent with a causal role for the loss of Nrxn2α in the genesis of autism-related behaviors, as suggested by the previous finding of deletions affecting exons of the NRXN2 gene in two unrelated individuals with autism.12, 13 Nrxn2α KO mice may thus provide a useful experimental system for the exploration of disease mechanisms and novel treatments in autism. The gene discussed is NRXN2; the disease is autism.