TRAP1 and neoplasm: Yoshida and colleagues showed that TRAP1 deficiency in immortalized mouse fibroblasts and in human tumor cells promotes an increase in mitochondrial respiration and fatty acid oxidation, and results in cellular accumulation of tricarboxylic acid cycle intermediates, ATP and reactive oxygen species; a basis for a mechanistic model for these regulations was provided by the finding that TRAP1 binds and consequently inhibits phosphorylation of mitochondrial cSrc, which is able to stimulate respiratory chain complex IV [7].