Invadopodia are actin-based membrane protrusions with high proteolytic activity that are thought to have an important role in cancer-cell invasion and intravasation. However, questions have remained about the formation and precise function of these structures during metastasis. On page 724, John Condeelis and colleagues extend their previous observation that neural Wiskott–Aldrich syndrome protein (N-WASP) is an essential component of invadopodia by discovering that N-WASP-mediated formation of invadopodia is required for the process of invasion and intravasation during breast cancer metastasis. Reducing the activity or expression of N-WASP in rat mammary adenocarcinoma cells leads to a reduction in the number and proteolytic activity of invadopodia in vitro, and decreases the invasive ability of the cells in vivo. The lack of functional N-WASP does not affect tumour size, but decreases the number of circulating tumour cells and the formation of metastasis. Primary tumour cells without functional N-WASP are also more round, less polarised, form fewer protrusions and are less mobile than cancer cells that express N-WASP. In addition, cells without N-WASP lack the ability to efficiently degrade collagen I at the invasive edge and in areas enriched with blood vessels. The actin nucleator N-WASP, thus, has a crucial role in driving the formation of proteolytic invadopodia and cancer cell metastasis.