Consistent with the in vitro findings, the results of in vivo studies indicated that large decreases in the tumor number, tumor burden, and EMT phenotype were caused by the TGFβ1 inhibitor disitertide in M+ EV-educated mice and that significant increases in the tumor number, tumor burden, and EMT phenotype resulted from exogenous Tgfb1 administration in mice treated with M− EVs (Fig. 8a–e). This evidence concerns the gene TGFB1 and neoplasm.