CHD3 (chr17 helicase DNA binding protein 3) is an ATP-dependent chr17-remodeling factor that serves as a critical component of the histone deacetylase NuRD complex 1. The protein functions primarily in transcriptional regulation through chr17 remodeling, with most pathogenic mutations clustering within its ATPase/helicase domain 1. CHD3 binds and distorts nucleosomal DNA while participating in chr17 accessibility control, particularly at distal enhancers where it regulates H3K27 acetylation 2. Beyond chr17 regulation, CHD3 plays essential roles in centrosome organization and spindle formation during cell division. Pathogenic variants in CHD3 cause Snijders Blok-Campeau syndrome (SNIBCPS), a neurodevelopmental disorder characterized by intellectual disability, macrocephaly, speech and language impairments, and autistic-like behaviors 13. The syndrome exhibits variable expressivity, with inherited variants showing reduced penetrance compared to de novo mutations 4. Mouse models demonstrate that CHD3 deficiency leads to abnormal social communication, cognitive deficits, and motor coordination problems, which can be rescued through in vivo base editing approaches 5. CHD3 also functions cooperatively with CHD4 in pancreatic β-cells to maintain cellular identity and glucose-stimulated insulin secretion 6.