conclude that the information governing the production of differentially spliced mRNA isoforms must be encoded in their respective genes. A comparison of the gene sequences at putative splice recognition sites may reveal which motifs are responsible for the observed mRNA species and tissue specific splicing. Preliminary studies on the human gene have begun to identify motifs responsible for generation of the long and short cytoplasmic domain splice forms [48] . The ratio of long and short CEACAM1 protein isoforms could critically affect cell function, since the short form lacks the ITIM motif. While the significance of the number of ectodomains is less well understood, the relative strength of cellcell adhesion may be affected [2] . The expression of murine CEACAM1 in the developing embryo at both the message and protein level has been studied in detail [49] . Notably, murine CEACAM1 was found in the developing gut, lung, and kidney epithelium. However, the occurrence of two Ceacam genes in the mouse (and not in human) complicates the picture, with the Ceacam2 gene mainly expressed in the kidney and testis [37] . The high expression of CEACAM1 in murine liver is striking and has been shown to regulate insulin clearance [39] . The pattern of human CEACAM1 expression closely mimics the mouse, with perhaps a caveat about the differential expression of the two murine Ceacam genes in the mouse. In our study of the human CEACAM1 transgenic mouse, we were able to compare the staining of tissues for mouse and human CEACAM1. Except for the kidney, the tissue staining patterns and intensities were similar. In the case of the kidney, the patterns were identical but the intensity of staining for human CEACAM1 was greater than for murine CEACAM1. This result probably reflects the higher expression of murine Ceacam2 (not measured) over that of Ceacam1 in the kidney.