The human ADH5 gene was reported to lack. the last exon compared to other mammalian ADHs and consequently should be expressed as a truncated protein. Here we show with PCR amplification of 3'-cDNA ends that the ADH5 gene harbors the "missing" exon. Besides a cDNA identical to the published sequence, we found full-length transcripts that contained additional codons for eight amino acid residues. Northern blot analysis established the full-length variant as the major transcript with the strongest signal from adult liver. Sequence analysis of genomic DNA confirmed that the ADH5 gene displays composite internal/terminal exons, which can be differentially processed; i.e., 3'-end generation is a result of competition between polyadenylation and splicing.