It is known that there is a significant decrease in ID3 after stroke, and from the correlation analysis it can be deduced that there is also a significant decrease in Claudin5, Occludin and ZO1, which is consistent with our knowledge that the massive damage to tight junction proteins after stroke leads to increased permeability of the vascular endothelium, which ultimately leads to massive infiltration of inflammatory factors [70, 71]. This evidence concerns the gene OCLN and stroke disorder.