When MOC31PE binds to EpCAM on the surface of cancer cells, it is internalized, upon which PE is cleaved off to cause inhibition of protein synthesis and induction of apoptosis.6,28 In addition to direct cell killing, we recently demonstrated that MOC31PE-induced cell death causes immune activation, measurable as a Th1 cytokine response, after intravenous administration to patients with end-stage metastatic CRC.8 In general, MOC31PE significantly enhanced a majority of local inflammatory/cytokine responses compared with CRS-HIPEC alone. This evidence concerns the gene EPCAM and cancer.