Li et al. (2013) studied ThVGdKO mice produced by genetic elimination of the genes for both vesicular transporters Vglut-1 and Vglut-2. In these mice thalamocortical glutamate neurotransmission in somatosensory cortex (but not in visual or auditory cortex) is silenced or knocked-out, thereby disabling the release of glutamate from synaptic vesicles. This resulted in a failure to construct barrel cortex columns, and induced severe defects in both cortical layer 4 lamination and in the morphology of spiny stellate cells. The authors explain this finding as follows: “We favor a model in which stellate neurons modulate activity and direct the local migration of neurons into barrels, modify gene expression, and influence cell morphologic development.” Li et al. (2013) present an hypothesis to explain their results: see also the preview of this paper by Barth and Kuhlman (2013). They suggest that it is possible that, by binding to its NMDA or metabotropic receptors, glutamate would stimulate second messenger chains that terminate by activating the appropriate transcription factors. We accept their hypothesis as a partial explanation, but we suggest that there may be other factors involved that they have not considered. To explain these more fully we add two additional hypotheses. These hypotheses are not competitive, either with each other or with the original hypothesis of Li et al. (2013), but constitute additions.