Regardless, the influence that Na,K-ATPase exerts over the aggressive behavior of these metastatic breast cancer cells along with the inflammatory co-regulation of sodium channels and sodium pumps, raises the possibility that the previously described effects of sodium channels on metastasis in cancer may not be due to direct VGSC activity but rather an indirect downstream effect on Na,K-ATPase. This evidence concerns the gene ATP12A and breast carcinoma.