Direct support for this idea comes from observations that reelin overexpressing mice have increased neurogenesis (Pujadas et al., 2010) and that exogenous reelin can recover cognitive deficits in mouse models of both Angelman syndrome and Alzheimers Disease (Pujadas et al., 2014; Hethorn et al., 2015). The gene discussed is RELN; the disease is early-onset autosomal dominant Alzheimer disease.