Adult neurogenesis occurs in a special microenvironment, named “niche” (Alvarez-Buylla and Lim, 2004; Lledo et al., 2006; Ming and Song, 2005; Ninkovic and Gotz, 2007; Zhao et al., 2008). Within the niche, a plethora of extracellular factors regulate adult neural progenitors and their development through activation of diverse intracellular signaling cascades (Schmidt and Duman, 2007; Zhao et al., 2008). How DISC1 participates in these signaling pathways in regulating different steps of adult neurogenesis is largely unknown. One clue came from studies of PTEN (phosphatase and tensin homolog deleted on chromosome ten), a lipid phosphatase that counteracts the kinase function of phosphatidylinositol-3-kinase (PI3K) and suppresses AKT activation (Maehama and Dixon, 1998). AKT is a major mediator of signaling pathways in response to a large spectrum of extracellular stimuli. Upon its activation in neurons, AKT phosphorylates different substrates, which in turn regulate diverse processes of neuronal development, including morphogenesis, dendritic development, synapse formation and synaptic plasticity (Atwal et al., 2000; Jaworski et al., 2005; Jiang et al., 2005; Kuruvilla et al., 2000; Markus et al., 2002; Sanna et al., 2002; Yoshimura et
