GSK3B and Alzheimer disease: While the functional contributions of CSD-induced ER stress and GSK-3β activation to CSD-induced AD pathogenesis, as well as the underlying mechanisms, remain to be elucidated, we tentatively suggest that induction of GSK‐3β activation or ER stress by CSD may not be the critical, sole effector of AD pathogenesis or a direct regulatory target of HBP/O-GlcNAc cycling under CSD conditions.