A series of studies have shown that the partial ablation of microglia in ganciclovir-treated CD11b-HSVTK mice (transgenic mice expressing thymidine kinase of Herpes simplex virus via the CD11b (Itgam) promoter; [159]), their partial deficiency in IL-34-/- mice [159] or their partial deficiency after treatment with a kinase inhibitor (PLX5622) that targets CSF1R [160] (Figure 5) can each accelerate CNS prion disease. Here, ITGAM is linked to prion disease.