1999) and positive clinical outcome (Jantscheff et al. 2003). The two CEACAMs are also expressed in a high proportion of tumor cell lines derived from breast, ovary, pancreas, prostate, and lung (Blumenthal et al. 2007; Beauchemin and Arabzadeh 2013). It has been proposed that CEACAM5/6 overproduction has a causative role in tumorgenesis, acting via an imbalance of cell surface adhesion molecules that disrupts differentiation, inhibits apoptosis and promotes both tumor formation and metastases (Ilantzis et al. 1997; Ordonez et al. 2000). This evidence concerns the gene CEACAM5 and neoplasm.