Researchers discovered that POGZ, the gene disrupted in White-Sutton syndrome, works as part of an epigenetic regulatory complex called PRC1.6 in developing brain cells. When POGZ was removed from mouse neuronal progenitor cells, hundreds of genes were dysregulated and critical neuronal genes failed to switch on properly. The study pinpoints a specific signaling pathway — bone morphogenetic protein (BMP) signaling — that is normally kept in check by POGZ and PRC1.6, and shows that disrupting this balance impairs the process of neurons maturing correctly. These findings help explain how POGZ mutations may contribute to neurodevelopmental conditions such as autism spectrum disorder and White-Sutton syndrome.