Given that there is anecdotal evidence of lorazepam (Ativan) causing rapid temporary improvement of ME symptoms, even in very severe cases, I’ve wondered why ME researchers aren’t looking more closely at researching selective translocator protein (TSPO) agonists. TSPO is also known as the peripheral benzodiazepine receptor (PBR) and is primarily found on the inner and outer mitochondrial membrane. A few selective TSPO/PBR agonist compounds exist in research, and they do not have affinity for the central GABAA receptor, therefore they do not have the negative effects benzodiazepines have so drugs selectively targeting TSPO could potentially be taken long term. A few examples are Ro5-4864, Emapunil, and SSR-180,575 By researching these compounds in ME/CFS we could discover if indeed the effect lorazepam has on ME symptoms is due to TSPO agonism and the resulting effects on mitochondria, glial cells, adrenals and steroids, inflammation, etc. and not due to central GABAA binding. In addition, these could be a tool to help us understand the pathophysiology of ME and a potential target for ME/CFS treatment and drug development.