These observations were important, as recent analyses of functions of the Arp2/3 complex activator Scar/WAVE in both B16-F1 mouse melanoma and Dictyostelium discoideum cells demonstrated that, in contrast to our JMY results, Scar/WAVE without its VCA domain still induced the formation of morphologically normal, actin-rich protrusions, extending at comparable speeds despite a drastic reduction of Arp2/3 recruitment21. The gene discussed is WASF1; the disease is melanoma.