In the C. elegans embryo, anterior-posterior polarity is defined at the one-cell stage, via asymmetric and reciprocal localisation of cortex-associated PAR protein complexes: PAR-3, PAR-6 and aPKC localise to the anterior, whereas PAR-1, PAR-2 and LGL-1 are enriched at the posterior. Polarity maintenance involves mutual antagonism between the anterior and posterior complexes and may also involve CDC-42-dependent regulation of myosin activity. Kenneth Kemphues and co-workers (p. 2005) now provide evidence for multiple and partially redundant pathways acting at the posterior to maintain polarity once it has been established. Both PAR-2 and CDC-42, acting in separate pathways, have dual functions in independently regulating both anterior PAR complex localisation and myosin activity, whereas LGL-1 appears to have a buffering role in controlling PAR-6 protein levels. Although the molecular details of these pathways remain incomplete, the complex and overlapping mechanisms operating to maintain polarity in the early embryo underscore the importance of robust and efficient polarisation for subsequent development.