Thus, in the presence of TAPI-0, the down-regulation of cell-derived sTNFR1 and sTNFR2 (and possibly also higher levels of TNFR1/TNFR2 left on the cell membrane) may stand in the basis of the increased ability of TNFα to induce the production of the pro-metastatic chemokines by the cancer cells. This evidence concerns the gene TNFRSF1A and cancer.