1994; Ashley, Kong et al. 1998; Ashley, Sampson et al. 1998; Jennings and Pietenpol 1998). Although TGF β has been shown to be an effective tumor suppressor in epithelial cells and in the early phases of tumorigenesis, once the tumor escapes its growth regulatory effect s, likely as the result of genetic instability, TGF β appears to function as a tumor promot er (Bierie and Moses 2006; Pardali and Moustakas 2007) by virtue of its involvement in all six of the essential hallmark cancer-related processes as defi ned by Hanahan and Weinberg (Hanahan and Weinberg 2000). The three known TGF β ligands (TGF β1-3) are ubiquitous and expressed in the majority of tumors (Arteaga 2006). T hese isoforms are highly homogenous in their mature regions with greater heterogene ity between their propeptide forms (Graycar, Miller et al. 1989) . Therefore, isoform specificity is likely controlled through propeptide sequences resulting in highly dynamic and spatially regulated expression. In addition to misregulation of the ligand, there are a variety of reported mutations and downregulation by hypermethylation of CpG islands in the receptors and Smads (Kim, Im et al. 2000; Levy and Hill 2006). Many tumors, including breast, col on, esophageal, gastric, hepatocellular, pancreatic, SCLC and NSCLC produce high levels of active TGF β isoforms (Constam, Philipp et al. 1992; Eastham, Tr uong et al. 1995; Friedman, Gold et al. 1995; Jakowlew, Mathias et al. 1995; Kong, Anscher et al. 1995; Yamada, Kato et al. 1995; Eder, Stenzl et al. 1996; Bier ie and Moses 2006; Levy and Hill 2006). Furthermore, overexpression of TGF β has been correlated with tumor progression and poor prognosis (Bieri e and Moses 2006; Levy and Hill 2006). Elevated TGFβ2 levels have also been linked with immunosuppression in both afferent and efferent limbs (Sporn, R oberts et al. 1986; Massague 1987; Bodmer, Strommer et al. 1989; Border and Ruosla hti 1992; Chen, Hinton et al. 1997; Bierie and Moses 2006; Li, Wan et al. 2006). Tumor-derived TGF β1 and PGE2 induce the upregulation of PD-L1 in imm unocompetent splenic dendritic cells and are causally related to the shif t in dendritic cell phenotype from immunostimulatory to immunosuppressive transgenic in the LSL-K-ras G12D/+p53loxP/loxP murine model of induced metastatic ovarian cancer(Scarlett, Rutkowski et al.). TGF β2 inhibits T cell activation in response to antigen stimulation as well as targeting cytotox ic T cell cytolytic pathways (Thomas and Massague 2005). Additionally, TGF β2 has antagonistic effects on the Natural Killer (NK) cells as well as the i nduction and proliferatio n of the lymphokine- activated killer (LAK) cells (Rook, Kehr l et al. 1986; Kasid, Bell et al.