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Background: Disabled-1 (Dab1) regulates laminar organization in the developing mammalian brain. Although mutation of the disabled-1 gene in scrambler mice results in abnormalities in neuronal positioning, migratory behavior linked to Dab1 signaling is not completely understood. Results outline the molecular mechanism by which Dab1 signaling controls the adhesive property of neurons to radial glia, thereby maintaining proper neuronal positioning during corticogenesis (1). Reelin is a large extracellular protein secreted by pioneer neurons that coordinates cell positioning during neurodevelopment. Dab1 is a phosphoprotein that appears to function as an intracellular adaptor in protein kinase pathways. Expression analysis indicates that mdab1 is expressed in neuronal populations exposed to Reelin. The similar phenotypes of reeler, scrambler, yotari and mdab1 null mice indicate that Reelin and Dab1 function as signaling molecules that regulate cell positioning in the developing brain (2). Layering of neurons in the cerebral cortex and cerebellum requires Reelin, Dab1 as well as two other proteins, cell surface receptors termed very low density lipoprotein receptor (VLDLR) and apolipoprotein E receptor 2 (ApoER2) (3).