In addition to increasing Aβ accumulation and promoting the formation of Aβ oligomers and neurofibrillary tangles, BIR also caused a surge in the activity of glycogen synthetase kinase-3β (73), phosphorylate tubulin associated unit excessively (74), thus became direct contributor to the progress of AD pathology. The gene discussed is KCNJ11; the disease is Alzheimer disease.