The TNF and TNF receptor gene superfamilies control a variety of distinct physiological functions such as cell proliferation, differentiation, and survival, etc. A newly emerging member this family with strong role in T cell homeostasis is GITR (glucocorticoid-induced tumor necrosis factor receptor) (Nocentini et al., 1998). A majority of glucocorticoid hormones are known to induce apoptosis (Nocentini et al., 1998). It is surprising to note that these hormones also protect the cells from undergoing apoptosis under the influence of discreet stimuli (Riccardi et a/., 1999). These events are thought to involve the participation of GITR and GILZ genes by controlling events like activation of NFkB and expression of Fas/ FasL molecules (Riccardi et al.. 1999). Recently, a human homolog of murine GITR was discovered (Kwon et al., 1999; Gurney et al., 1999). The human receptor was called AITR (activation-induced TNFR member) (Kwon et al., 1999) and hGITR (Giirney et al., 1999). Its ligand was cloned and called AITRL (Kwon et al., 1999) and hGITRL (Gurney et al., 1999). Within the cytoplasmic domain, the AITR shares a striking homology with 4-1BB and CD27 (Kwon et al., 1999). AITR associates with TRAF1 (TNF receptor-associated factor 1). TRAF2. and TRAF3. and induces NFkB activation via TRAF2 (Kwon et al., 1999). AITRL was expressed in endothelial cells (Kwon et al., 1999). Expression of GITR appears to be activation dependent as stimulation of T lymphocytes by anti-CD3 mAb. Con A, or phorbol 12-myristate 13-acetate plus Ca-ionophore treatment readily upregulates its levels (Nocentini el aLs 1997).