It was shown that overexpression of TOM40 improves the mitochondrial function and efficiency, abolishes the Aβ mitochondrial toxicity [109], possibly by improving import of repair enzymes and antioxidants [110], produced in cytoplasm and transferred to mitochondria [111], via dicarboxylate carrier (DIC) [112] and TOM40 pores [113], which in AD may be blocked by Aβ oligomers [114]. This evidence concerns the gene SLC25A10 and Alzheimer disease.