Abnormally increased dendritic spine turnover has been observed in several autism mouse models (Chow et al., 2009; Jiang et al., 2013; Isshiki et al., 2014; Gdalyahu et al., 2015), including the MECP2-duplication, neuroligin-3, 15q duplication, PTEN, and CNTNAP2 mice, suggesting they share a deficit in the balance between structural synaptic plasticity and stability. This evidence concerns the gene PTEN and autism.