Coincidental alterations of K-Ras and p16INK4A were mainly found in M+ tumours (2/67 M− tumours vs 17/139 M+ tumours; P=0.034), suggesting that abnormalities in these pathways could cooperate for a more aggressive phenotype, as previously supported by Serrano et al (1997). This evidence concerns the gene CDKN2A and neoplasm.