Although these studies are useful as a proof of principle that apoptosis negatively regulates protective immune responses mediated by T cells, pharmacological and genetic ablation of apoptosis pathways during infection opens a “Pandora box” of undesirable effects such as the onset of autoimmunity in gld/lpr models (65–67) or increased inflammation in the hearts of T. cruzi-infected mice treated with anti-FasL (58). The gene discussed is FASLG; the disease is infection.