The data therefore establish fenofibrate as a potent inhibitor of VEGF-dependent angiosarcoma cell proliferation and highlight important pharmacological differences with its observed effects in other cancer cells in terms of potency, effects on apoptosis and mitochondrial function, PPARα- and NFκB-dependence, and interactions with PPARα- and NFκB pathways. Here, NFKB1 is linked to angiosarcoma.