Other reports have shown that CD34 + cells decreased sustained pro-inflammatory activity of NF-κB and its downstream effector molecules TNF-α, IL-1β, and IL-6 at the wound bed of diabetic NOD/SCID mice.68 Additionally, angiogenesis marker VEGFr1 expression were significantly higher in IC and IA cell-treated groups than vehicle-treated stroke animals but not IN. This evidence concerns the gene CD34 and stroke disorder.