The key question, which Manczak’s group attempted to answer with a very interesting study, is how much VDAC1 is minimally sufficient to reduce the extent of the interaction between VDAC1 and Aβ and between VDAC1 and P-tau in order to maintain synaptic activity, mitochondrial function, and neuronal survival in the brains of transgenic mice with AD [47]. This evidence concerns the gene MAPT and Alzheimer disease.