The metastatic process is complex, requiring invasion, haematogenous and/or lymphatic dissemination, angiogenesis, colonization of a distant site and avoidance of host immune responses. These phenotypic changes can be accomplished by a variety of molecular pathways. Recent evidence suggests that many of the genetic events required for metastatic competence can be coordinately regulated, perhaps by regulatory cascades controlling normal development and differentiation. In addition to alterations in cellular phenotypes, metastatic cells also exhibit genomic instability, the causes of which are presently unknown. The development of therapeutic strategies to counteract metastasis may be most promising if directed towards the final angiogenesis and colonization by tumour cells at the metastatic site. Such strategies must overcome the redundancy of molecular mechanisms.