Although increased [18F]-PRB111 uptake has been demonstrated in several animal models of neurological diseases including epilepsy [144, 145], multiple sclerosis [146], and schizophrenia [147], these models display extensive inflammation and postmortem pathology [144–147], whereas abnormalities in the HIV-1 Tat transgenic mouse model are more subtle [148] with opioid exposure inducing modest gliosis [29, 149]. This evidence concerns the gene TAT and epilepsy.