Several studies have demonstrated that sFasL acts as a Fas-dependent chemotactic agent for neutrophils in non-apoptotic pathways (Ottonello et al., 1999; Seino et al., 1998), and sFasL levels are increased in patients with autoimmune diseases, graft-versus host disease, and cancer (Das et al., 1999; Hashimoto et al., 1998; Murayama et al., 1999). Here, FASLG is linked to graft versus host disease.