Recently, we demonstrated that CSF-1R inhibition–induced microglia/macrophage depletion could be tracked using an 18F-labeled radiotracer—N,N-diethyl-2-(2-[4-(2-fluoroethoxy)phenyl]-5,7-dimethylpyrazolo[1,5-α]pyrimidine-3-yl)acetamide (18F-DPA-714)—targeting the translocator protein (TSPO) (7): TSPO-dependent neuroinflammation was significantly decreased within the first weeks after stroke, although long-term CSF-1R inhibition was associated with a poor disease outcome. This evidence concerns the gene CSF1R and stroke disorder.