RE:RE:RE:RE:News Release On the other hand, the anti-inflammatory properties of the Avn analog Tranilast have been attributed mainly to its capacity to inhibit the release of chemical mediators from mast cells and basophils [34, 55], suppress COX-2 and iNOS expression [56], and limit TNFα-induced secretion of IL-6 and surface expression of vascular adhesion molecules, including VCAM-1, ICAM-1 and E-selectin, in endothelial cells by inhibiting NF-κB-dependent gene transcription [38]. Furthermore, Tranilast anti-inflammatory properties were shown to be triggered by the induction of HO-1 expres- sion via ERK1/2 activation [55]. Finally, recombinant YAvns were demonstrated to downregulate NF-κB and rescue inflammatory phenotypes in cellular and animal models of CCM disease [41] (Table 2).