Inhibition of this proteolytic activity with selective GCPII inhibitors has been shown to be neuroprotective in experiments with mouse models 12; NAAG activation of metabotropic glutamate type 3 receptors exerts neuroprotective effects toward glutamate‐mediated excitotoxicity caused by elevated levels of glutamate released during stroke, traumatic brain injury, and other pathological conditions 13, 14, 15. Here, FOLH1 is linked to stroke disorder.