However, our study suggests that the neuroprotective effect of Hesperidin in the in vitro AD model–characterized by decreased levels of Aβ1–42 and phospho-Tau (T181), enhanced ADAM10 gene expression, and suppressed BACE1 gene expression–is probably mediated by a mechanism other than CK2 inhibition. The gene discussed is BACE1; the disease is Alzheimer disease.