A research has shown that EA could inhibit Toll-Like Receptor 4 signaling and up-regulate Transient Receptor Potential Vallinoid 1 in sensory neurons to attenuate paclitaxel-induced peripheral neuropathic pain in rats.[39] Other research have shown that EA could attenuate cancer-induced bone pain via NF-κB/CXCL12 signaling in midbrain periaqueductal gray,[15] and changes in protein phosphorylation in the dorsal root ganglia of EA-treated BCP (bone cancer pain) rats indicate that mTOR signaling may be a key point in the alleviation of BCP.[40]. This evidence concerns the gene NFKB1 and cancer.