Autism spectrum disorder is a prevalent developmental disorder with neurological origins. ASD symptomatology includes abnormalities in social and communicative behavior, cognitive impairment, and comorbid epilepsy and insomnia. It is often characterized by sleep difficulties and estimates hold that insomnia affects 40-80% of children in the ASD population. This study aims to determine if the 16p mouse line is a valid ASD mouse model for studying sleep. This study also aims to show the 16p mouse line exhibits similar sleep disturbances (like sleep fragmentation and increased awakenings) to those seen clinically in ASD patients. The 16p knockout mouse has a deletion at chromosomal region 16p11.2, and studies have shown they display hyperactivity and sex-related bias of sleep symptoms. Using electroencephalogram (EEG) and electromyography (EMG) recordings of 16pxB129 mice and controls, with 24-hour baseline recordings, this study found that 16p deletion mice have increased microarousals during NREM sleep resulting in sleep fragmentation. 16pxB129 mice also displayed weaker infraslow rhythm during baseline recordings, which may be related to the consistency of their sleep cycle. However, the neural mechanisms underlying various sleep disturbances in ASD are not well studied. A future direction this study could take is to examine the neural circuit mechanisms contributing to this sleep fragmentation in 16p mice.