In prior work, we identified bioenergetic deficits in cortical synaptic mitochondria from APP-SAA knock-in mice, a genetically faithful model of AD, which were linked to hyperphosphorylation of CRMP2 and its dissociation from the ANT [20], a key component of the mitochondrial PTP [31,32,33,34,35]. The gene discussed is DPYSL2; the disease is Alzheimer disease.