In previous investigations, we focused on the structural and functional determinants of tumor suppression mediated by CEACAM1-4L, one of two major splice variants expressed in rat liver [13, 16] . The primary goal in these studies was to gain insight into the role of the cytoplasmic and extracellular domains in cell adhesion and tumor suppression. In the present report, we have focused on the CEACAM1 transmembrane domain, a relatively uncharacterized region shared by both the 4L and 4S isoforms. Our cell model for these studies was an anchorage dependent, CEACAM1 negative subclone designated 253-NT that was derived clonally from the parental rat 253T cell line [6] . When suspended in soft agar, 253T cells continued to grow and by three weeks had formed well-defined anchorage independent colonies ( Figure 1A ). In comparison, soft agar cultures of 253-NT cells showed no evidence of significant growth and after three weeks were composed almost entirely of single cells ( Figure 1B) . In contrast, 253-NT cells stably transfected with a wild type CEACAM1-4S expression plasmid and enriched by FACS to yield cultures at least 70% positive for CEACAM1-4S expression regained the anchorage independent phenotype of the parental 253T cells ( Figure 1C ) while cells stably transfected with empty vector ( Figure 1D ) had not grown significantly after 3 weeks in soft agar.