These transcripts are of great interest because not only were they cancer specific (only found in poorly differentiated Mahlavu and SK-Hep1 cells) and relatively abundant (30 and 70% of the isolated CAD cDNA clones, respectively), but they also preserved the CAD domain (aa 1–80) directing CAD interaction with its inhibitor (ICAD) (Mukae et al, 1998; Uegaki et al, 2000, Otomo et al, 2000). This evidence concerns the gene CAD and cancer.