Autism Spectrum Disorders (ASDs) are neurodevelopmental conditions characterized by impairments in social interaction and repetitive behavior. Abnormalities in synaptic function and resultant memory deficits have been frequently associated with ASDs. In this study, we examined a possible association between impaired memory formation and the candidate disease-associated mutations on the POGZ (Pogo transposable element with ZNF domain) gene. We found that the freezing time was significantly lower in a mouse model heterozygous for a Q1038R mutation in POGZidentified in a patient with ASDs (POGZ-Q1038R mice) 24 hours after electric foot shock in the fear-conditioning contextual learning task. We also found that POGZ-Q1038R mice showed significantly less interest in the novel object than wild-type mice. These results suggest that the ASDs-associatedPOGZ-Q1038R mutation causes impaired memory formation. Further studies on the molecular, cellular, and neural-circuit level mechanisms of impaired memory formation caused by the POGZ-Q1038Rmutation will help to clarify the pathogenic mechanism of memory impairment in patients with ASDs.