Accordingly, at 1% O2 leukemic B cells markedly increase glycolysis as evaluated both through the dynamic monitoring of metabolic responses and the expression of glycolysis genes such as those encoding the glucose transporter GLUT1 (SLC2A1), LDHA, the lactate transporter monocarboxylate transporter 4 MCT4 (SLC16A3), and PKM2. Once again, this effect is partly mediated through the activation of ADO signaling, as indicated by the complete reversion of the glycolytic behavior of CLL cells upon the addition of A2A inhibitor, directly linking ADO signaling to central metabolic programs. This evidence concerns the gene SLC16A3 and B-cell chronic lymphocytic leukemia.