Intriguingly, p16Ink4A seems to play an opposite role in lung non-neuroendocrine carcinomas, with the percentage of cases displaying the entire spectrum of p16Ink4A positivity significantly higher in well/moderately differentiated tumors (41.3%) compared to poorly differentiated and undifferentiated malignancies (26.1%).These results confirm that CDKN2A deregulation through distinct mechanisms, including rare point mutations, promotor methylation and frequent homozygous deletions, is a relatively frequent event occurring in non-small cell lung cancer [18]. This evidence concerns the gene CDKN2A and non-small cell lung carcinoma.