CASP2 and neoplasm: This is in strong contrast to the opposing effects of its putative interaction partners, Caspase-2 or Pidd1.3, 4 Hence, the function of Raidd as a ‘direct activator of Caspase-2' needs to be re-considered, at least in the context of Eμ-Myc-driven tumorigenesis and justifies the search for additional activators as well as substrates of Caspase-2 to understand its tumor-suppressive function at the molecular level.