microRNA-9-2andmicroRNA-9-3double-mutant mice demonstrate thatmicroRNA-9(miR-9) controls neural progenitor proliferation and differentiation in the developing telencephalon by regulating the expression of multiple transcription factors. As suggested by our previous study, the Foxg1 expression was elevated, and the production of Cajal-Retzius cells and early-born neurons was suppressed in themiR-9-2/3double-mutant pallium. At embryonic day 16.5 (E16.5), however, the Foxg1 expression was no longer elevated. The expression of an AU-rich RNA-binding protein Elavl2 increased at E16.5, Elav2 associated withFoxg13′ untranslated region (UTR), and it countered theFoxg1suppression by miR-9. Later, progenitor proliferation was reduced in themiR-9-2/3double-mutant pallium with the decrease in Nr2e1 and Pax6 expression and the increase in Meis2 expression. The analyses suggest thatmicroRNA-9indirectly inhibitsPax6expression by suppressing Meis2 expression. In contrast, together with Elavl1 and Msi1,microRNA-9targetsNr2e1mRNA 3′ UTR to enhance the expression. Concomitantly, cortical layers were reduced, each cortical projection was malformed, and the tangential migration of interneurons into the pallium was impaired in themiR-9-2/3double mutants. miR-9 also targetsGsh23′ UTR, and Gsh2, as well as Foxg1, expression was elevated in themiR-9-2/3double-mutant subpallium. The subpallium progenitor proliferation was enhanced, and the development of basal ganglia including striatum and globus pallidus was suppressed. Pallial/subpallial boundary shifted dorsally, and the ventral pallium was lost. Corridor was malformed, and thalamocortical and corticofugal axons were misrouted in themiR-9-2/3double mutants.