Hazlett et al. (2011)showed that early brain enlargement typical of autism may be associated with increased surface area overgrowth due to faulty cell adhesion. One such mechanism would be faulty adhesion molecule β-catenin, a component of the cadherin protein complex that constitutes adherens junctions. Adhesion molecules are thought to reduce growth of brain progenitor cells. APP modulates β-catenin degradation in vitro and in vivo (Chen and Bodles, 2007). Evidence also suggests that molecular defects in autism interfere with synaptic protein synthesis (Kelleher and Bear, 2008). The gene discussed is CDH17; the disease is autism.