Cyclin-dependent kinase inhibitors (CKIs) play important roles in embryonic development by directly inhibiting the cell cycle machinery to promote cell cycle exit and limit tissue growth. The Drosophila CKI Dacapo (Dap) contributes to normal cell cycle exit in multiple developmental contexts, including the embryonic epidermis, nervous system, and eye. Because of its function as a potent cell cycle inhibitor, altered Dap expression can significantly disrupt normal development. For example, in the embryonic epidermis, premature Dap expression can induce early cell cycle exit, while the absence of Dap expression leads to delayed cell cycle exit and inappropriate cell division. Thus Dap expression must be carefully controlled to ensure normal tissue growth and differentiation. Indeed, multiple mechanisms have been shown to contribute to the regulation of Dap expression, including transcriptional regulation via a complex cis-regulatory region, miRNA-mediated translational inhibition, and regulated proteolysis via interaction with the CRL4Cdt2 ubiquitin ligase. We have further examined the role of miRNA-mediated regulation of Dap expression in the embryonic epidermis. We have found that a dap transgene expressed under the control of the endogenous cis-regulatory region but lacking the endogenous 3’UTR is expressed prematurely in the embryonic epidermis. In addition, miRNA “sensor” transgenes that include the dap 3’UTR are repressed in comparison with controls. Finally, embryos lacking expression of a miRNA known to bind the dap 3’UTR, miR-7, exhibit premature dap expression. Future experiments will continue to explore the functional significance of miRNA-mediated repression of Dap expression in the embryonic epidermis.