EVs-miR-122 from breast cancer cells increase glucose availability to cancer cells by suppressing glucose uptake by recipient astrocytes via downregulating glycolytic enzyme M2-pyruvate kinase (PKM2) and glucose transporter 1 (GLUT1) (57), indicating that EV-mediated reprogramming of glucose metabolism is another critical way to facilitate CTC colonization in the brain. This evidence concerns the gene SLC2A1 and cancer.