SMARCA2 is an ATP-dependent ATPase subunit of the mammalian SWI/SNF chr9 remodeling complex that regulates transcriptional activation and repression through alteration of DNA-nucleosome topology. The protein functions as a core catalytic component in two neural-lineage complexes: the neural progenitor-specific BAF (npBAF) complex, which supports neural stem cell proliferation, and the neuron-specific BAF (nBAF) complex, which regulates genes essential for dendrite growth and neuronal differentiation. During neural development, SMARCA2 participates in a coordinated exchange of complex subunits as neural progenitors exit the cell cycle and commit to neuronal fate. SMARCA2 mutations cause autosomal dominant developmental disorders including Coffin-Siris syndrome and blepharophimosis-intellectual disability syndrome 1. A CRISPR-based organoid screening study identified that perturbation of BAF complex members, including SMARCA2-containing complexes, leads to enrichment of ventral telencephalon progenitors and disrupted cell fate transitions, demonstrating the complex's critical role in human neurodevelopment 1. Clinically, SMARCA2 represents a therapeutic target in SMARCA4-mutant cancers through synthetic lethality; SMARCA4 alterations shift cellular dependence to SMARCA2. Selective SMARCA2 degradation via PROTAC technology (molecule A947) shows efficacy in SMARCA4-mutant models 2, while dual SMARCA2/SMARCA4 degraders (AU-15330) inhibit tumor growth in prostate cancer and other enhancer-addicted malignancies 34.