Although Claspin expression can be exploited by cancer cells for their survival, Claspin’s role as an oncogene should be regarded with caution since, generally, its expression and activation only seem to reflect and be secondary to triggering of oncogene-induced pathways, to the ongoing RS, and to the acquisition of stemness features (e.g., CD44, CD133, and ALDH expression) [97,98]. This evidence concerns the gene PROM1 and cancer.