periventricular and callosal points of introduction, in advancing waves that seem to repulse resident murine progenitors, which then die, both in situ and upon retreat to the cortical surface (Figure 2). The human GPCs ultimately attain a relatively uniform distribution, achieving apparent contact inhibition in a manner analogous to that reported developmentally by Bergles and colleagues (Hughes et al. 2013). While the molecular basis for the competitive dominance of the human GPCs is unknown, several recent studies have identified differential expression of both MYC and hedgehog-dependent pathways as contributing to clonal dominance during early ontogeny (Amoyel and Bach 2014; Amoyel et al. 2014; Claveria et al. 2013). Further assessment of differential gene expression by mouse and human GPCs in vivo may permit the discovery of similar regulators of competition that favor the relative dominance of human over mouse GPCs when the two are in direct competition, a decidedly unnatural situation that might nonetheless provide us important insights into the differential expansion of favored glial cell populations in the developing human brain, and the signals that determine which among competing populations is ultimately dominant.
