To observe the physiological roles of p16Ink4a and p21Waf1/Cip1 during tumour formation, we previously generated transgenic mice lines expressing firefly luciferase under the control of the p16Ink4a or p21Waf1/Cip1gene promoters; these were termed p16-luc or p21-luc mice, respectively, and we revealed the timing, and hence, the likely roles of p16Ink4a and/or p21Waf1/Cip1 expression in de novo tumorigenesis in vivo10,11. This evidence concerns the gene CDKN2A and neoplasm.