ZMYND11 encodes a histone reader protein that functions as a transcriptional corepressor, primarily through recognition of H3K36me3 histone modifications and control of transcription elongation 1. It acts as an epigenetic regulator that can eject the elongation corepressor from actively transcribed genes 1, while also regulating brain-specific RNA splicing through RBFOX2 to control developmental pathways 23. Beyond its canonical histone-reading role, ZMYND11 exhibits noncanonical function as a reader of arginine-methylated HNRNPA1, restricting stress granule formation and tumor progression 4. Pathogenic variants in ZMYND11 cause autosomal dominant syndromic intellectual disability characterized by developmental delay with speech impairment, behavioral abnormalities, seizures, and hypotonia 56. Loss-of-function mutations disrupt cortical neurogenesis by inappropriate upregulation of latent developmental pathways in neural stem cells 23. ZMYND11 variants also associate with autism, aggression, and complex neuropsychiatric features 5, and represent a genetic risk factor for schizophrenia 7. Clinically, ZMYND11-related disease presents with distinctive dysmorphic features and potentially metabolic complications 68. The homogeneous phenotype likely results from common loss-of-function mechanisms 6.