The Drosophila wing primordium is a simple epithelial structure with significant regenerative capacity. As in any regenerative system, it is essential to maintain correct tissue size and shape during the repair process, yet little is known about the mechanisms that enable such control. In this issue (p. 3541), Florenci Serras and colleagues demonstrate that regeneration of the Drosophila wing involves respecification of cell fate as well as reorientation of cell division in order to drive intercalary growth. Following genetic ablation of wing cells, the authors observed a respecification of vein and intervein fates, which was independent of Hedgehog and Decapentaplegic morphogen activity. The authors identified the proteins Fat (Ft) and Crumbs (Crb) as required for the reorientation of cell division, and showed that mutations in ft or crb lead to misorientation of the mitotic spindle as well as to Yorkie-driven excessive proliferation, resulting in malformed wings. This elegant Drosophila model provides novel insight into the mechanisms of epithelial regeneration and wound repair.