Alzheimer's disease (AD) is the most prevalent neurodegenerative disease characterized by memory deficits and cognitive decline. It is mainly characterized by two neuropathological features -the accumulation of extracellular amyloid β (Aβ) protein plaques and neurofibrillary tangles primarily composed of hyperphosphorylated Tau protein. Majority of cases of AD are known to be sporadic in nature, however, a small percentage of cases are familial (known as Familial AD or FAD), caused by dominant autosomal mutations found in one of three genes: presenilin-1 (PSEN1), and presenilin-2 (PSEN2), and amyloid precursor protein (APP). Sun et al. knocked out PSEN1 genes using CRISPER/Cas9 in mouse neuroblastoma cells and this decreased the production of Aβ42 and Aβ40. suggests that the CRISPR/Cas9 approach can be used to selectively disrupt the PSEN1M146L allele responsible for AD, and partly switch the abnormal Aβ42/40 ratio that leads to the development of the disease in carriers of this mutation. Ortiz-Virumbrales et al. demonstrated that CRISPR/Cas9 can correct neurons derived from the PSEN2N141I mutated individual fibroblasts and can further normalize the Aβ42/40 ratio. This was shown to effectively restore the associated electrophysiological deficits.