CAPZA2 encodes the α2 subunit of the CapZ F-actin capping protein complex, a critical regulator of actin cytoskeleton dynamics 1. The protein binds to the barbed ends of actin filaments in a calcium-independent manner, blocking subunit exchange without severing filaments, thereby stabilizing F-actin and regulating actin polymerization and depolymerization 1. CAPZA2 functions in diverse cellular contexts: it interacts with SEPTIN10 to support actin stress fiber formation and mechanotransduction signaling that activates oncogenic YAP/TAZ pathways in hepatocellular carcinoma 2, and associates with CFTR to regulate its plasma membrane stability under EPAC1 activation in epithelial cells 3. Dysfunction of CAPZA2 is linked to neurodevelopmental disorders. Heterozygous de novo CAPZA2 mutations cause global developmental delay, intellectual disability, motor development impairment, hypotonia, and seizures in children 14. A novel splicing variant (c.219+1 G>A) causing exon 4 skipping has been documented 4. Additionally, CAPZA2 emerges as a potential biomarker in comorbid type 2 diabetes and major depressive disorder, with upregulation in disease models 5, and as a candidate biomarker in primary open-angle glaucoma pathogenesis 6. CAPZA2 dysregulation also occurs in mesenchymal tumors through novel fusion events 7.