In nervous system diseases, studies have shown that loss‐of‐function mutations in maternal UBE3A account for 8% of Angelman syndrome (AS) cases [8], while hyperactivity of UBE3A accounts for 1–3% of autism spectrum disorder (ASD) cases worldwide [9, 10] and sometimes leads to increased nonproteolytic ubiquitylation of ALDH1A proteins, which compromises retinoic acid (RA) biosynthesis and impairs the activity of neurons [11]. Here, UBE3A is linked to Angelman syndrome.