The tumor suppressor gene CDKN2A is functionally inactivated, through mutations, deletions, or methylation, in a large variety of primary neoplasms as well as tumor cell lines. The CDKN2A locus gives rise to two distinct transcripts. P16INK4 and P19ARF. Because it has been shown that the disruption of only P19arf-coding sequences in mice is sufficient for tumor development, this transcript most likely also encodes a tumor suppressor. We have analyzed the two CDKN2A transcripts in fifteen human primary liver carcinomas, two human hepatoma cell lines, and five rodent hepatoma cell lines. No homozygous deletions of P19ARF and P16INK4 were found in these samples, whereas the normal P19arf transcript was absent in two of the five rodent cell lines (nonexpressed in one case and mutated in another). These results suggest that functional abrogation of P19ARF is not a primary event in hepatocarcinogenesis.