For example, targeted CRISPR/Cas9 editing of the glia maturation factor (GMF) gene in microglia led to reduced GMF expression and suppressed microglial activation, as evidenced by decreased p38 MAPK phosphorylation and proinflammatory cytokine production in vitro, supporting the potential for microglia-targeted gene editing to attenuate neuroinflammation in Alzheimer’s disease models [61]. The gene discussed is GMFB; the disease is early-onset autosomal dominant Alzheimer disease.