This together with the observed beneficial neurologic effects by neflamapimod suggests that chronic inflammation may play a role in this rat tMCAO stroke model. This is a finding that supplements previously reported IL-1 results in this type of model [36,73,74]. Although this single time point analysis appears to exclude a neflamapimod effect on IL-1 production, it does not necessarily preclude a neflamapimod effect on IL-1 signaling, even though a correlative relationship of the Day 44 IL-1 levels with the six-week mNSS values or with their Day 44 BDNF levels was not found. The present study was not intended to address the exact mechanism of action of neflamapimod and the IL-1 and BDNF **data** are very limited.