The pharmacological and genetic intervention towards the T. cruzi proapoptotic effect against effector T cells is desirable; nevertheless, unintended effects have been observed, such as the development of autoimmunity in models using FasL-deficient (gld) or Fas-deficient (lpr, lymphoproliferative) mice [141–143], as well as heightened cardiac inflammation in T. cruzi-infected mice treated with anti-FasL antibodies [144]. This evidence concerns the gene FASLG and Autoimmunity.