As evidence of a tight link between Moesin and cell cycle activation, we observed presence of Moesin in every incidence of PCNA positivity in brains of tau transgenic Drosophila. Taken together, this series of experiments suggest that the Moesin elevation we observe in human Alzheimer’s disease is indeed a consequence of pathogenic forms of tau and correlates with actin over-stabilization and cell cycle activation. The gene discussed is MSN; the disease is early-onset autosomal dominant Alzheimer disease.