The three major cell types of the mammalian central nervous system are all derived from neural precursor cells (NPCs). The undifferentiated state of NPCs is maintained by Notch signalling and secreted growth factors; NPCs divide a fixed number of times before differentiating to ensure that the brain contains the right mix of cells. Now, on p. 2553, Yoshimatsu and colleagues report that STAT3 (signal transducer and activator of transcription 3) acts in a non-cell-autonomous manner through the Notch ligand Delta-like 1 (DLL1) to maintain NPCs in the embryonic mouse neocortex. They show that NPCs express STAT3 and that deletion of Stat3 in a subset of cells in vivo and in vitro produces premature neurogenesis in their neighbours. STAT3, they report, regulates the expression of DLL1. Moreover,the knockdown of DLL1 by RNAi blocks the ability of STAT3 to maintain NPCs. The authors suggest that this previously unrecognized interaction between STAT3 and Notch signalling might maintain other stem cell populations during development.