SMARCC2 is a core component of the BAF (BRG1/BRM-associated factor) chr12 remodeling complexes that regulate transcription through ATP-dependent alterations of DNA-nucleosome topology 1. It stimulates ATPase activity of catalytic complex subunits 2 and participates in both transcriptional activation and repression 3. SMARCC2 exists in neural progenitor-specific (npBAF) and neuron-specific (nBAF) complexes, which undergo subunit exchange during neural differentiation to regulate genes essential for dendrite growth and neuronal commitment. In myeloid lineages, SMARCC2 controls granulocytopoiesis and neutrophil granule gene expression. Phosphorylation of SMARCC2 regulates neuronal differentiation 4. Pathogenic variants in SMARCC2 cause Coffin-Siris syndrome 8, a neurodevelopmental disorder characterized by intellectual disability, hypotonia, and behavioral issues 5. Loss-of-function variants are inherited with mild cognitive effects, while de novo missense variants cause severe developmental delay through distinct pathomechanisms 5. In cancer, SMARCC2's role is context-dependent: it suppresses breast cancer tumorigenesis through chr12 accessibility modulation 6, yet promotes triple-negative breast cancer progression within specific SWI/SNF complex assemblies 7, and supports pancreatic cancer metastasis when stabilized 8.