The thalamus relays information to the cortex and consists of dozens of distinct groups of neuronal cell bodies called thalamic nuclei. How do these separate nuclei form during development? On p. 1317, James Li and co-workers use an inducible genetic fate-mapping technique to demonstrate the importance of the homeobox transcription factor Gbx2 in the differentiation of thalamic nuclei. By tracing the fates of Gbx2-expressing cells and their descendants, the authors establish that these cells contribute to all thalamic nuclei, but that the precursors of different nuclei express Gbx2 at different times during development. Interestingly, Gbx2 seems to control this segregation of cells into different thalamic nuclei by acting on postmitotic neurons. The researchers also show that although the loss of Gbx2 does not lead to any obvious patterning defects in the forebrain, it results in disrupted dorsal and posterior thalamic boundaries, which normally separate the thalamus from neighbouring brain structures. From this and other data, the authors propose that Gbx2 functions cell-nonautonomously in regulating thalamic boundary formation.