MES eGBOs had high activity of the HMGA2(+) regulon, which promotes GBM stemness, invasion and in vivo tumor formation[36] (Figure 2G), while PRO eGBOs had high activity of the FOXJ3(+) regulon, which is a neuroectodermal TF recently identified as a GBM‐driving gene.[37] Together, these results demonstrate that underlying differences in gene regulatory networks alter the neural development of eGBOs and promote an oncogenic transcriptional landscape. The gene discussed is HMGA2; the disease is glioblastoma.