In contrast to the rapid early-onset weight gain seen in ob/ob mice (1-3), mutations in the tub gene lead to obesity gradually and strongly resemble late-onset obesity as seen in the human population (4). In addition to excessive deposition of adipose tissue, mice with the tub phenotype also suffer retinal degeneration and neurosensory hearing loss (4-6). The tripartite character of tubby phenotype is strikingly similar to human obesity syndromes such as Alstr鰉 (5) and Bardet-Biedl (6). A candidate for the tub gene has been described (4). A G芓 transversion in this candidate gene eliminates a donor splice site in the 3' coding region resulting in a larger transcript containing an unspliced intron (4). A second prematurely truncated mRNA transcript with the unspliced intron was found to be expressed in the brains of tubby mice at a 2-3 fold higher rate as compared to B6 mice (4). It has been postulated that the phenotypic features of tubby mice can be attributed to cellular apoptosis triggered by the expression of a mutated tub gene (4).