Based on all the above, we hypothesize the mechanism of celastrol protects against cerebral I/R injury may be attributed to the decrease in sulfatide, which consequently inhibits sulfatide-triggered elevated expressions of NF-κB, p-JNK, and p-c-Jun, thus ultimately reduces ischemic stroke-induced cell apoptosis. This evidence concerns the gene NFKB1 and ischemic stroke.