Antioxidants augment tumor vascularity in vivo in a BACH1‐dependent manner, and BACH1 overexpression increases the sensitivity of tumor cells toward anti‐angiogenesis therapy.[54] On the contrary, only one report showed that BACH1 decreases the protein levels of HO‐1, p‐AKT, p‐ERK, eNOS, HIF1α, and VEGF, and inhibits angiogenesis in pancreatic cancer cells.[220] In ischemia‐induced angiogenesis of adult mice, BACH1 exerts its effect in inhibiting angiogenesis in endothelial cells under the condition of increased oxidative stress, which is different from the role of BACH1 in tumor cells. This evidence concerns the gene AKT1 and familial pancreatic carcinoma.