Retinal hypoxia, activation of HIF1α, and consequent expression of angiogenic factors are crucial for the development of diabetic retinopathy.[15, 18] Thus, to further investigate TRAP1‐dependent retinal vascular changes in vivo, retinal hypoxia and HIF1α stabilization were examined in a streptozotocin (STZ)‐induced mouse model of type 1 diabetes[19] (Figure S6A,B, Supporting Information). The gene discussed is HIF1A; the disease is diabetic retinopathy.