We further investigated the role of CEACAM1 in ammonia-mediated disruption of TGF-β signaling, by examining p-SMAD3 in SW480 human colon cancer cells after overexpressing either full-length CEACAM1 (CEACAM1-FL) or a C-terminal deletion mutant lacking the ITIM motif (CEACAM1-ΔC) (Fig. 5, A and B). Here, SMAD3 is linked to colonic neoplasm.