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Autism spectrum disorder (ASD) is a frequent neurodevelopmental disorder characterized by variable clinical severity. Core symptoms are qualitatively impaired communication and social behavior, highly restricted interests and repetitive behaviors. Although recent work on genetic mutations in ASD has shed light on the pathophysiology of the disease, classifying it essentially as a synaptopathy, no treatments are available to date. To develop and test novel ASD treatment approaches, validated and informative animal models are required. Of particular interest, in this context are loss‐of‐function mutations in the postsynaptic cell adhesion protein neuroligin‐4 and point mutations in its homologue neuroligin‐3 (NL‐3) that were found to cause certain forms of monogenic heritable ASD in humans. Here, we show that NL‐3‐deficient mice display a behavioral phenotype reminiscent of the lead symptoms of ASD …