The 5th highly cited article established a programmed cell death protein 1 null mutation in 2C T cell receptor transgenic mice of the H-2b/d background and revealed that the mice developed chronic and systemic GVHD.[33] The 9th most cited article showed that CD4+CD25+ T cells are strong regulators of GVHD versus conventional donor T cell-mediated graft versus tumor activity.[34] Finally, some articles were based on clinical treatments and clinical reports,[35,36] namely, the 3rd and 4th highly cited articles, which focused on the clinical aspects of GVHD therapy. This evidence concerns the gene CD4 and neoplasm.