As previous studies have shown that increased filopodia number and length upon EGF and TGFβ stimulation promote invasiveness of cancer cells30,31 and DOCK4/RAC1 control lateral filopodia formation25, we quantified the number of filopodia on breast cancer cells cells upon EGF and TGFβ stimulation and their potential dependence on DOCK4/RAC1 (Fig. 3d, g, h). The gene discussed is EGF; the disease is breast carcinoma.