Current testing systems including karyotype analyses, FISH, comparative genomic hybridization, or PCR to check for tumor marker expression may not be sensitive enough to detect the expected low proportion of affected cells [72], but even occurrence of alterations, like aneuploidity does not predict transformation, as recently demonstrated by Tarte et al. These data nevertheless helped to refine control assays, easily to perform, to control cell cycle/senescence and transformation pathways by, for example, PCR for p14, p16Ink4a, p21, p53, hTERT, and oncogenes like c-myc. This evidence concerns the gene CDKN2A and neoplasm.