Sun et al. reported that in a ubiquitin E3 ligase, UBE3A ubiquitinates LAMTOR1, resulting in its proteasomal degradation, and Lamtor1 knockdown in hippocampal CA1 neurons of mice with Angelman syndrome reduces elevated mTORC1 activity and improves dendritic spine maturation, long-term potentiation, as well as learning performance [83]. This evidence concerns the gene LAMTOR1 and Angelman syndrome.