More recently, this idea has been expanded by the Steeg lab that reports that NM23-H1 interacts with Dynamin in MDA-MB-231 breast carcinoma cells and the above mentioned NDPK contribute to suppression of tumor cell motility by promoting endocytosis of chemotactic receptors by facilitating Dynamin oligomerization and increasing its GTPase activity [91]. The gene discussed is NME1; the disease is breast carcinoma.