Based upon this study, we propose that AD pathogenesis may be related to abnormality of signal transduction (AGTR1 and PTAFR), decrease in protein transport capacity (COL5A2 (221729_at), COL5A2 (221730_at), COL4A1), impairment of axon repair (CNR1), and intracellular calcium dyshomeostasis (CACNB2, CACNA1E). The gene discussed is CACNA1E; the disease is Alzheimer disease.