In addition to its pivotal role in neuronal survival, PI3K/Aktsignaling is integral to neuronal differentiation and neuriteoutgrowth. However, the exact role of Akt in neuronaldifferentiation is still controversial. Here, we found thatnuclear expression of CA-Akt resulted in unusual rapid neuriteoutgrowth and overexpression of KD-Akt caused multipledendrite growth without specific axon elongation. Moreover,microarray data revealed that the expression of FOXQ1expression was about 10-fold higher in cells with nuclear,active Akt than in control cells. Quantitative real-time PCRanalysis showed that mRNA levels were upregulated inNLS-CA-Akt cells as compared to KD or EV cells. Furthermore,our FACS analysis demonstrated that overexpression ofNLS-CA-Akt accumulate cells in the G1 phase within 24 h,fitting with the rapid sprouting of neuritis. Thus, our dataimplied that at least in this early time frame, the overexpressionof nuclear, active Akt forced cells into neurite developmentthrough probably FOXQ1regulation.