In HUVECs, which express high levels of ecto-ATP synthase, angiostatin inhibited cell proliferation and ATP production, but was not cytotoxic [10]; in A549 lung cancer cells, both angiostatin and a polyclonal anti-ATP5B antibody blocked ATP synthesis, induced intracellular acidification, and triggered cell death [68]. Here, ATP5F1B is linked to lung cancer.