Consistent, with this notion a dominant-negative RAB35S22N mutant abrogated PDGF-induced CDRs formation and directional migration (Supplementary Figure 3D), whereas two recently identified activated, tumour-associated RAB35 mutants, RAB35A151T and F161L48, promoted CDRs formation and elevated AKT phosphorylation in the absence of growth factor stimulation (Supplementary Figure 3E and Movie 16). The gene discussed is AKT1; the disease is neoplasm.