The impairment of motility of microglial processes that occurs in some pathological conditions, e.g., in models of Alzheimer’s disease with amyloid β plaque deposition (Koenigsknecht-Talboo et al., 2008, Krabbe et al., 2013, Condello et al., 2015) raises the question of whether the dependence of surveillance on THIK-1 activity can be employed therapeutically. This evidence concerns the gene KCNK13 and early-onset autosomal dominant Alzheimer disease.