HIF‐1α is activated by the chemical inducer CoCl2, which forces cancer cells to adapt to a hypoxic environment, speeding up VM formation and EMT.10 In our CoCl2‐induced hypoxia cell model, we confirmed that overexpressing TP53INP1 hindered breast cancer invasion and the formation of VM vessels; hypoxia‐induced breast cancer cells overexpressing TP53INP1 had decreased expression of VM and EMT‐related proteins. Here, HIF1A is linked to breast cancer.