Previous studies have reported that inflammation following traumatic brain injury persists for a long time after the primary insult.20 In this regard, BEVs play a pivotal role in worsening inflammation in distal tissues.21 To determine whether BEVs were involved in exacerbating postinjury inflammation, we labeled CD63 (a marker of EVs) with L1 cell adhesion molecule (L1CAM, a marker of the neural region) and characterized BEVs in tendons derived from the different groups. Here, CD63 is linked to injury.