Consistent with previous findings that the expression of Nav1.8 mRNA and protein are increased within lumbar 4–5 DRG in an animal model of bone cancer pain [10], our present study provide additional direct evidence demonstrating a functional upregulation of voltage-gated sodium channel subtype Nav1.8 on the membrane of DRG neurons in a rat cancer pain model, which is proved to be required for the development of cancer-induced bone pain. Here, SCN10A is linked to cancer.