Since our in vitro results showed that the PLC pathway, activated by Dex via CXCR4 [19], strongly regulated mitochondrial function and Dex sensitivity, we next examined whether the effect of CXCR4 inhibition on Dex-induced B-ALL apoptosis [19] was mediated through the modulation of mitochondrial functions. The gene discussed is HSPG2; the disease is precursor B-cell acute lymphoblastic leukemia.