Since overexpression of the anion channel causes apoptosis, and high VDAC1 levels have been found in post-mortem AD brains and in amyloid precursor protein (APP) transgenic mice, it has been hypothesized that VDAC1 may cause neuronal cell death characteristic of AD; therefore, VDAC1 targeting would represent a new way to inhibit neuronal cell death in AD [17]. The gene discussed is APP; the disease is Alzheimer disease.