This is in line with what recently reported by Götzl et al. [86], showing that loss of TREM-2 enhances the expression of genes associated with a homeostatic microglial state in vivo, contrarily to the neurodegenerative microglial phenotype, which derives from the ablation of progranulin (GRN), an additional gene involved in neuroinflammation occurring in AD and FTD. The gene discussed is GRN; the disease is Alzheimer disease.