Exploration of expression of prominent cytokines in tumor bearing and tumor-immunized mice which might affect tumor growth confirmed, as expected, an increased presence of IL-6 and IL-17 (Figure 3). While TNFα expression was similarly enhanced, we have been unable to modulate tumor invasion in vitro or growth in vivo by targeting TNFα [7]. Following growth of both tumors in vivo we also recorded enhanced expression of TGFβ in DLN (Figure 3). There are intriguing other research data showing the complexity of interactions which can modulate tumor cell growth/invasion-thus cancer cell escape from TGFβ-induced cell suppression can be modified by targeting another site of immunotherapy, namely simultaneous use of checkpoint inhibitors, such as PD-1/PD-L1 antibodies. The anti-tumor effect of the combination of PD-L1 antibody and TGF-β antibody is reported to be greater than that seen with single-drug treatment [37,38]. Data in Figures 4 and 5 support the hypothesis that TGFβ may be a crucial factor implicated in the enhanced EMT6 tumor invasion seen in the presence of IL-6/IL-17, which is attenuated by immune DLN (Figures 3 and 4). Thus addition of anti-TGFβ reduced the suppression by immune DLN cells of invasion of EMT6 induced by IL-6/IL-17. Furthermore, addition of recombinant TGFβ itself decreased invasion of EMT6 induced by IL-6/Il-17 (Figure 5). Note that for the highly inflammatory tumor 4THM, antiTGFβ and recombinant TGFβ had, if anything, the opposite effects (Figures 4D and 5B). There was a trend to augmented tumor invasion induced by TGFβ, and towards attenuation of invasion in the presence of anti-TGFβ, which we suggest is most with a primary effect of TGFβ in this tumor on enhanced EMT and invasion [26,39]. This, in turn, is further consistent with our in vivo data indicating that attenuation of an inflammatory response by the CD200:CD200R axis played no major role in control of growth/metastasis by 4THM, unlike EMT6.