Indeed, Zhang et al. demonstrated in diabetic mice and in albumin-treated proximal tubular HK-2 cells how anomalies resulting from diabetes, e.g., hyperglycemia and ROS, can mediate the overexpression or overactivation of the dipeptidyl peptidase-4 (DPP4) enzyme, leading to DPP4-mediated cleavage of stromal cell-derived factor-1α (SDF-1α) and suppression of the SDF-1α/C-X-C Motif Chemokine Receptor 4 (CXCR4) phosphorylation of STAT3 at the level of serine-727. This evidence concerns the gene DPP4 and Hyperglycemia.