 NAV3 is a gene that is commonly mutated or deleted in human tumors. It has been found to be involved in the dissemination of primary tumor cells through its ability to regulate epithelial migration and invasion. When induced by growth factors, NAV3 localizes to the plus ends of microtubules and enhances their polarized growth. This leads to longer microtool growth, which in turn extends the duration of growth factor signaling, prevents apoptosis, and increases random cell migration. Mathematical modeling suggests that NAV3-depleted cells have an advantage over those without it due to their ability to explore their environment more efficiently. In animal models, silencing NAV3-increased metastasis, while ectopically expressing the wild type form had the opposite effect. Additionally, analysis of greater than 2,500 breast and lung cancer patients showed that low levels of NAV3 were associated with shorter survival times. These findings suggest that NAV3 plays a role in regulating the directionality of migrating cells, thereby reducing the risk of metastasis. This article was authored by Harder's Co and Vashi, Nibbentetrit, Waslin-Vussell, and others.