Our data support a model in which KLF4 is activated in GSC downstream of the MAPK pathway in part through EGR1, and we further demonstrate that EGR1 acts as a transcriptional regulator of KLF4 in GSCs in-vitro, and its expression level positively correlates with KLF4 in clinical GBM tumor samples. The gene discussed is EGR1; the disease is neoplasm.