Lastly, our work may have direct relevance to certain human epithelial cancers, such as lung cancer or glioma, where overexpression of ECT2/Pbl has been reported to correlate for poor prognosis 92, 93, and where our findings suggest it could drive not only disruption of epithelial polarity via activation of Cdc42 or Rac 94, 95 but also loss of adherens junctions via sustained Rho activation to promote tumour progression. The gene discussed is ECT2; the disease is central nervous system cancer.