The establishment and maintenance of cell polarity—that is, the asymmetrical partitioning of cellular materials—is fundamental to stem‐cell renewal and development. The budding yeast Saccharomyces cerevisiae is a leading model organism for studying cell polarity. Yeast cell polarity is intimately connected to the organization of the actin cytoskeleton, which guides secretion towards the budding site or tip of the growing bud, resulting in polarized cell growth (Pruyne et al , 2004). Pioneering work by Lew & Reed has established roles for cyclin‐dependent kinases (CDKs) and their cyclin partners in cell polarity; at the time of bud emergence, G1 cyclins trigger polarized growth, whereas mitotic cyclins reverse this effect during mitosis. Inactivation of CDK following mitosis triggers redistribution of the actin cytoskeleton to the neck region for cytokinesis (Fig 1; Lew & Reed, 1993). The role of G1 cyclins in cell polarity has been known for more than ten years but the lingering problem has been the identity of their targets. Three recent studies published in The EMBO Journal (Knaus et al , 2007; Sopko et al , 2007; Zheng et al , 2007) and one in Nature Cell Biology (McCusker et al , 2007) have significantly advanced our understanding of the important substrates of G1 cyclin–CDK and their interesting mechanisms of action. Figure 1. Cell‐cycle regulation of cell polarity in budding yeast. Polarized growth sites (red), where Cdc42 is presumably active, change during the cell cycle. These changes are brought about by the action of G1 cyclin bound to cyclin‐dependent kinase (CDK) and mitotic cyclin–CDK activity. In some environments, Candida albicans keeps its polarized status and develops highly polarized hyphae. For cell polarization, cell division cycle (Cdc) 42 is the ‘Rome to which all roads lead’. Cdc42 is a Rho‐type small GTPase, the activity of which is regulated in budding yeast by a single guanine‐nucleotide …