The present invention relates to variants of TRAF2 which demonstrate the ability to inhibit the TNF signaling path-way. In particular, applicants have isolated a splice variant of TRAF2 referred to hereinafter as "TRAF2 truncated" or "TRAF2TR" and a TRAF2 expression construct with enhanced dominant negative properties, hereafter referred to as "TRAF2 truncated-deleted" or "TRAF2TD". Both TRAF2TR and TRAF2TD have the ability to inhibit the TNF signaling pathway and in TRAF2TD, this ability is greatly enhanced, greatly reducing the response to TNF binding.