This pathway, supported by consensus L-R-TFs inference and causal network modeling, highlights CEBPD as a master regulator of hypoxia-regulated invasion and stemness in GBM, corroborating studies where CEBPD augments extracellular matrix-integrin interactions and promotes glioma stem-like cell maintenance, thereby enhancing TMZ resistance (41, 42). This evidence concerns the gene CEBPD and glioma.