A growing body of evidence indicates that CAP exposure effectively abrogates the free and membrane-associated isoforms of tNOX [39,89,90,91,92,93,94,95], either in the serum of patients with active cancer through supramolecular interactions [89] or in cancer cell cultures, through the depletion of its transcriptional regulator [83] POU domain, class 3 transcription factor 2 (POU3F2). The gene discussed is ENOX2; the disease is cancer.