That no difference of p16 expression was seen between cancers with and without heterozygous 9p deletion demonstrates that breast cancer cells are able to fully compensate for loss of one p16 (CDKN2A) allele, either by increased transcriptional activation of the remaining allele or by increased stabilization of p16 protein or mRNA (reviewed in [5, 25]). This evidence concerns the gene CDKN2A and breast carcinoma.