It is known that, modulation of TLR9 function, via CpG ODN agonists, showed amelioration of CAA levels, cortical amyloid burden in association with behavioral improvements in animal models of AD [16–19, 22], with a non-negligible safety profile in non-human primate model of sporadic AD pathology [22]. The gene discussed is TLR9; the disease is amyloidosis.