The discrepancy of our Drosophila results and the established upregulation of Mena in cancer can be due to the following: dysregulation of actin skeleton by Mena knock-down in eyeful and sensitized flies may lead to increased metastasis and neoplasia due to lack of proper cell attachment and increased cell motility, whereas high levels of Mena in many human cancers could be due to the fact that overexpression of Mena leads to overactivation of growth factor signalling and therefore cells overexpressing Mena would be predominant in certain tumors. The gene discussed is ENAH; the disease is neoplasm.