An innovative study employing CRISPR/Cas in an induced pluripotent stem cell (iPSC) model differentiated to microglia, demonstrated that TREM2-KO reduces microglial survival, alters its phagocytosis function, and results in an impaired response to beta-amyloid plaques, thus revealing possible mechanisms that may have an essential role in AD progression (McQuade et al., 2020). This evidence concerns the gene TREM2 and Alzheimer disease.