Discovery of the mitochondrial function of Fhit in apoptosis, through interaction with Fdxr, extends functional parallels of tumor suppressors, Fhit and p53, lost sequentially in most cancers and involved in response to DNA damage, with p53 acting as a transcriptional and Fhit a posttranscriptional Fdxr regulator. Here, FDXR is linked to neoplasm.