However, mounting evidence indicates that soluble dimeric and oligomeric Aβs are more neurotoxic than insoluble deposits.12,13,20 It has been shown that amyloid plaque burden has poor correlation with Alzheimer’s disease severity.12,13,20 Nonetheless, in the past few decades, insoluble Aβ (insAβ) plaques have been the primary target for AD drug design and clinical trials, and this could partially explain the failures of AD drug development. The gene discussed is DDX41; the disease is Alzheimer disease.