Actually, CRP as common clinical indicator of inflammatory status could upregulate the VEGF-A expression by activating hypoxia inducible factor-1alpha in adipose-derived stem cells.[29,30] Furthermore, disruption in immune homeostasis with a shift toward a Th2-dominant or chronic inflammatory state by tumor-derived VEGF has been reported previously.[31] By contrast, we noticed that the Th1/Th2 immune imbalance with a shift to a Th1-dominant was associated with plasma VEGF accumulation in T2DM. This evidence concerns the gene CRP and type 2 diabetes mellitus.