SLC2A1 and neoplasm: Sarrazy et al. (2016) suggest that increased glucose transporter 1 (Glut1) -dependent glucose uptake is associated with increased bone marrow hematopoiesis and monocytic generation, subsequently leading to macrophage-dependent atherosclerotic plaque formation. Su et al. (2016) found that EMMPRIN interacts with Glut1 in A375 cells, reducing glucose uptake and inhibiting tumor cell proliferation.