Previous studies have shown that gene expression of CX3CL1 is regulated by TNF-α in other cell types [56], that CX3CL1 inhibits neuronal death by reducing the production of pro-inflammatory cytokine via inhibition of LPS-induced microglial activation [57,58,59], and that stem cells genetically modified to overexpress CX3CL1 exhibited enhanced neuroprotective effects, and reduced ischemia-induced cerebral infarct size and neurological deficits [60,61]. Here, TNF is linked to cerebral infarction.