**1. Introduction**

During neural induction, the ectoderm stem cells overlying the notochord of the mesoderm convert into neuroepithelial cells (NECs) that proliferate/differentiate rapidly to form neural plate in response to diffusible inhibitory signals (neural inducer) produced from the noto‐ chord. Neural plate folds to form neural groove, which fuses to form neural tube. Within the neural tube, NECs undergo asymmetric dividing to generate neural stem cells (NSCs, or called radial glia cells) due to the expression of B-cell translocation gene 2 (BTG2) [1, 2, 3, 4]. NSCs differentiate sequentially into neural progenitor cells (NPCs) and various lineage-re‐ stricted neural blast cells, which include neuroblast and glioblast. These neural blast cells migrate to the target region where they mature and integrate into the existing neural net‐ work [5]. The generation of different lineage occurs in a temporally distinct yet overlapping pattern. In rodents, neuronogenesis peaks at embryonic day (E) 14, astrocytogenesis at post‐ natal day (P) 2, and oligodendrocytogenesis at P14 [6, 7]. It remains largely unclear at which step the fate of neuronal lineage has been decided, from embryonic stem (ES) cells to NECs, to NSCs and to terminally-differentiated neurons. The transcriptional factor NFκB plays a pivotal role in inflammation, immunity, cancer and neural plasticity [8, 9]. Constitutive and inducible activation of NFκB has been reported in many types of human tumors and chronic diseases including neurodegenerative diseases [10, 11, 12, 13, 14]. However, moderate acti‐ vation of NFκB signaling on many physiological conditions may benefit the whole process of neuronal fate decision, including neurodevelopment and adult neurogenesis [15].
