Combined with our previous conclusion that TXL is capable of suppressing leukocyte‐endothelial cell interactions in ischemic stroke mice,7 we herein hypothesize that leukocyte‐endothelial cell interactions mediated by numerous adhesion molecules and chemokines are an important cause of no‐reflow after vascular recanalization in ischemic stroke, and TXL can alleviate the no‐reflow by inhibiting these biological targets. Here, TXNL1 is linked to ischemic stroke.