Although, the results in human patients are somewhat conflicting [35–38,40–43] most studies indicate that NOD2 acts as a negative regulator of inflammation, since SNPs 8, 12, 13 and other similar nod2 variants, in both donor and recipient correlate with acute and chronic GVHD increased severity, non-relapse mortality, epithelial disease and overall survival [43]. The gene discussed is NOD2; the disease is chronic graft versus host disease.