Autism spectrum disorders (ASD) are composed of a range of conditions affecting the development of the nervous ststem; these groups of disorders are unified by characteristic impairments in social interaction, communication, and repetitive behaviors. Due to the somewhat hetereogeneous nature of these conditions, several environmental and genetic causes have been associated with ASD. Among the genetic causes, the CNTNAP2 gene is implicated in syndromic forms of ASD. As such, this gene has been studied in the context of animal model systems, primarily mice and rats; these studies have indicated that knockout of the CNTNAP2 gene results in features that are similar to that observed in human ASD. To further assess this animal model of ASD, in this study, we assessed the behavioral phenotypes of CNTNAP2 knockout mice using a range of behavioral assays targeting core and comorbid traits of ASD. We confirmed that CNTNAP2 mutant mice exhibited social interaction deficits, reduced ultrasonic vocalizations, repetitive behaviors, and hyperactivity, aligning with core and comorbid ASD features. Notably, we also identified novel findings: CNTNAP2 knockout mice displayed increased rearing behavior and lacked anxiety-like behaviors, diverging from the assumption that anxiety is a common feature of this model. These results demonstrate that CNTNAP2 knockout mice recapitulate key ASD-related behaviors while highlighting novel behavioral aspects; these data reinforce their utility as an animal model for studying ASD.