We further investigated the role of GABPA in controlling cell migration and demonstrate that although ELK1 and GABPA ultimately control the same biological process, they do so by regulating largely distinct transcriptional programmes. The ETS-domain transcription factors are an excellent model to study how individual members of transcription factor families can elicit specific biological effects. Several genome-wide ChIP analyses have shown that different members of this family show broad overlaps in the genomic regions to which they bind. However, despite these overlaps, there are groups of binding regions that appear to be uniquely bound by one or a limited subset of family members, and it is thought that it is through these regions that the specific regulatory activities of individual family members are elicited. Indeed, we recently showed that in breast epithelial MCF10A cells, the ETS protein ELK1 binds in a ‘unique’ manner to a set of binding regions, and through these sites, it regulates the expression of a set of genes that are ultimately involved in controlling cell migration. There is another set of ELK1 binding regions that, in another cell type, can also be occupied by a different ETS protein, GABPA, and these regions are not generally associated with genes involved in the migratory properties of these cells. Thus, it was assumed that GABPA would not control cell migration in MCF10A cells but instead would drive different biological processes. Here, we demonstrate that although GABPA likely affects many different biological processes, contrary to expectations, it also plays an important role in controlling cell migration. However, GABPA and ELK1 control cell migration through directly regulating the expression of different profiles of CYT387 supply target genes. Thus in this case, they ultimately converge to control the same biological process. Previous studies on GABPA have hinted at a role in controlling cell migration. For example, it was shown that depletion of GABPA reduced the migratory properties of vascular smooth muscle cells. These effects on migration were attributed to its role in controlling the expression of the kinase KIS, and the subsequent effects on phosphorylation and activity of the cell cycle inhibitor p27. However, here we have shown a wider role of GABPA in controlling the expression of genes directly involved in controlling cell migration. In the same study, depletion of GABPA in MEFs reduced the numbers of cells entering the cell cycle, which is consistent with previous work that implicated GABPA as a key controller of cell cycle progression. We also find that in MCF10A cells, GABPA plays an important role in controlling the activity of a programme of genes involved in cell cycle control and it appears to do this by both indirect and direct mechanisms. In keeping with this finding, depletion of GABPA in MCF10A cells leads to changes in their overall cell cycle distributions. In another study, the analysis of the entire GABPA regulome led to the identification of many of the functional categories that also appear in our data as potentially directly regulated by GABPA such as “transcriptional regulators” n addition to “cell cycle regulation”. However, by further subpartitioning GABPA targets according to regulatory mode, our study provides further insight and suggests that many of these categories are upregulated by GABPA activity. Indeed, overall the predominant mode of action for GABPA appears to be as a transcriptional activator. Conversely, we show that GABPA depletion also causes upregulation of gene expression, implying a repressive role, even in the context of direct target genes.