The metastatic tumor model displayed a greater loss of stress ligands (ULBP1, MICA), downregulation of chemokine expression (MCP-1), and higher production of inhibitory soluble molecules (i.e., TGF-β, IL-6), as compared with a non-metastatic tumor model, more resembling the in vivo scenario. This evidence concerns the gene TGFB1 and neoplasm.