Cell polarity is thought to generate cell fate diversity through asymmetric cell divisions, but which components of polarized cells convert polarity information into cell fate determination? On p. 4297, Sergei Sokol and co-workers report that the answer in Xenopus epidermal ectoderm is the conserved polarity proteins atypical protein kinase (aPKC) and partitioning-defective 1 (PAR1). Early asymmetric divisions in Xenopus embryos produce superficial (apical) and deep (basal)ectodermal layers. These contain superficial epidermal cells and ciliated cells, respectively. In gain- and loss-of-function studies, the researchers show that aPKC, which is localized to the apical domain of the superficial cells, inhibits ciliated cell differentiation and promotes superficial cell fates. aPKC, they report, phosphorylates PAR1 and targets it to the basolateral domain of the superficial cells and PAR1, they show, stimulates ciliated cell differentiation and inhibits superficial epidermal cell fates,possibly through Notch signalling. This aPKC/PAR1 pathway, the researchers suggest, may link cell polarity to cell fate determination in epithelial tissues in many species.