This further supports the results of our own previous work and the data reported by others indicating that the tumour-suppressive function of p16INK4a is exclusively abrogated in (pre-)neoplastic but not in merely inflammatory or hyperproliferative conditions (Barrett et al, 1996; Hsieh et al, 1998; Klump et al, 1998). Here, CDKN2A is linked to neoplasm.