Recently, Chang and colleagues derived neurons from fAD patients with APP D678H mutation and reported aberrant accumulation of intracellular and secreted Aβ1–42 and Aβ1–40 peptides, increased activation of GSK3β, hyperphosphorylation of Tau, impaired neurite outgrowth, downregulation of synaptophysin, and increased caspase 1 activity. The gene discussed is APP; the disease is familial Alzheimer disease.