A critical event in early mammalian development is the generation of inside cells, which develop into the inner cell mass (ICM) and ultimately the embryo itself, and outside cells, which form the trophectoderm. Before this cell-fate decision can occur, the blastomeres have to develop cell polarity and the ability to divide asymmetrically, events that are regulated in many invertebrate embryos by the Par (partitioning defective) molecules and atypical protein kinase C (aPKC). On p. 505, Magdalena Zernicka-Goetz and colleagues show for the first time that a similar molecular mechanism regulates asymmetrical cell division in vertebrate embryos. They report that downregulation of Par3 or aPKC function by injection of double-stranded RNA directed against Par3 or mRNA encoding a dominant-negative form of aPKC, respectively, into random blastomeres in 4-cell stage mouse embryos changes the fate of the injected cell's progeny by directing them towards the ICM. This partitioning, the authors report, is achieved by increasing the frequency at which the progeny divide asymmetrically and by decreasing their probability of retaining outside positions.