Furthermore, the overexpression of the soluble form of TNFR2 (sTNFR2) or the membrane form of TNFR2 in human or rat BM-MSCs enhanced their therapeutic effects in murine models of RA [34, 35] and cardiac ischemia [36, 37], which was associated with reduced TNF, IL-1β, and IL-6 secretion. This evidence concerns the gene TNFRSF1B and myocardial ischemia.