The role of FasL in the induction of apoptosis by T. cruzi has also been corroborated with the use of an antibody anti-FasL that blocked apoptosis induction in CD8+ T lymphocytes, increased T cell proliferation, improved the Th1 response that restored macrophage-mediated immunity to T. cruzi infection, and diminished peak parasitemia [135, 140] (Figure 2c). This evidence concerns the gene FASLG and parasitic infectious disease.