For instance, cytotoxic T lymphocytes, CD4+ and CD8+, are the major effectors of GVHD and cause tissue damage by a variety of pathways including: the Fas-Fas ligand (FasL) and perforin-granzyme pathways [43], TNF-receptor (TNFR)-like death receptors such as TNF-related apoptosis-inducing ligand (TRAIL) and TNF-like weak inducer of apoptosis (TWEAK) [44,45,46,47,48]. Here, FASLG is linked to graft versus host disease.