Qin et al show that autism-like social deficits in Shank3-deficient mice arise from β-catenin-mediated transcriptional upregulation of histone deacetylase 2 (HDAC2) and are persistently alleviated by brief treatment with HDAC inhibitor romidepsin.
- Luye Qin
- Kaijie Ma
- Zhen Yan