In addition, RNA-seq analysis and further studies revealed that the underlying mechanism of neuroprotective and functional improvement after iTBS was closely related to the modulation of microglial activation by shifting the M1/M2 phenotype balance in peri-infarcted area during the course of stroke via inhibiting TLR4/NFκB/NLRP3 signaling pathway, which may contribute to preventing the pyroptosis associated inflammatory response. Here, TLR4 is linked to Stroke.