Reciprocal interactions among GSCs require the activation of multiple pathways that promote tumor propagation including metabolic reprogramming for the hypoxia niche and autophagy pathway, Notch signaling, basic fibroblast growth factor (b-FGF), secretion of vascular endothelial growth factor (VEGF), stromal cell-derived factor 1 (CXCL12) with activation of the membrane-associated receptor CXCR4 [39,40], and activation of hypoxia-inducible factor (HIF2α) [41,42]. Here, FGF2 is linked to neoplasm.