Although most of the literature points out a neuroprotective role of BET inhibition in AD, a very recent report demonstrated that inhibition or degradation of BET protein BRD4, obtained by treatment with JQ1 and ARV-825, respectively, enhanced Tau hyperphosphorylation and Aβ levels as a result of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) activation in H4-APP751 human neuroblastoma and 3D-AD human neural cell culture. Here, BACE1 is linked to Alzheimer disease.