The immune T-cell compartment maintains the capability to respond to a wide variety of antigens (Ag). This whole process is regulated by lymphocyte apoptosis (programmed cell death, PCD) and involves the coordinated expression of a great number of genes including those coding for cytokines and their receptors, such as for example IL-2/IL-2R and the Fas/FasL systems and those coding for transcription factors, including the NF-kB complex, involved in T-cell activation and apoptosis in that they simultaneously activate cell suicide and an anti-death programme. This binary effect, PCD activation and inhibition, is due on one hand to GCH-induced activation of the caspases cascade and on the other to the induction of expression of a new gene that we have named GILZ. In fact, GILZ over-expression in transfected cells inhibits the sequential increase of NF-kB/DNA-binding activity, IL-2 production and IL-2R expression, and transcription of the Fas/FasL complex that follows TCR triggering and plays an important role in the control of T-lymphocyte apoptosis. These results indicate a new mechanism responsible for the GCH-mediated inhibition of T-cell death and activation that could contribute to anti-inflammatory and immunosuppressive efficacy.