The transcription factor MafA regulates glucose-responsive expression of insulin. MafA-deficient mice have a normal proportion of insulin⁺ cells at birth but develop diabetes gradually with age, suggesting that MafA is required for maturation and not specification of pancreatic β-cells. However, several studies show that ectopic expression of MafA may have a role in specification as it induces insulin⁺ cells in chicken gut epithelium, reprograms adult murine acinar cells into insulin⁺ cells in combination with Ngn3 and Pdx1, and triggers the lens differentiation. Hence, we examined whether MafA can induce specification of β-cells during pancreatic development. When the MafA transgene is expressed in Pdx1⁺ pancreatic progenitors, both pancreatic mass and proliferation of progenitors are reduced, at least partially due to induction of cyclin kinase inhibitors p27 and p57. Expression of MafA in Pdx1⁺ cells until E12.5 was sufficient to cause these effects and to disproportionately inhibit the formation of endocrine cells in the remnant pancreas. Thus, in mice, MafA expression in Pdx1⁺ pancreatic progenitors is not sufficient to specify insulin⁺ cells but in fact deters pancreatic development and the differentiation of endocrine cells. These findings imply that MafA should be used to enhance maturation, rather than specification, of β-cells from stem/progenitor cells.