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defects that result from either miR-184 overexpres-small RNAs, including microRNAs (miRNAs), in stem cell regu-lation (Liu and Zhao, 2009; Shen and Temple, 2009). AlthoughZhao, 2008). Deciphering these regulatory mechanisms repre-sents a step toward understanding the plasticity of adult brains and realizing the therapeutic potential of adult neural stem cells. regulates the expression of miR-184 in aNSCs, and high levels of miR-184 promoted aNSC proliferation and inhibited differenti-ation both in vitro and in vivo. We further identified NumblikeEpigenetic mechanisms, including DNA methylation and histone modification, are known to play significant roles in the modulation of stem cell proliferation and differentiation (Li and (Numbl) as a downstream target of miR-184, and exogenously expressed Numbl could rescue aNSC proliferation and differen-tiation deficits resulting from either elevated miR-184 or MBD1sion or MBD1 deficiency. Therefore, MBD1, miR-184, and Numbl form a regulatory network that helps control the balance between proliferation and differ-entiation of aNSCs