ADAM10/SAP97 interaction is reduced in AD patients' hippocampi at Braak 4, suggesting a SAP97 cargo dysfunction in the pathology.7 Therefore, we asked whether an alteration of PKC phosphorylation at the residue T629 of SAP97 could be responsible for the decrease in ADAM10/SAP97 association in AD patients. The gene discussed is ADAM10; the disease is Alzheimer disease.