In a subsequent study, the same authors provided evidence that the CXCL12–CXCR4/CXCR7 axis exerts its action in thyroid cancer cells by increasing their migration and invasiveness via Akt (also known as protein kinase B) and extracellular signal-regulated kinase signaling, and by activating matrix metalloproteinase-2 (40). This evidence concerns the gene AKT1 and thyroid cancer.