To address this risk, researchers are developing methods to mitigate the risk of GVHD, such as using gene-editing approaches to delete or downregulate genes that are involved in T cell activation and proliferation, such as CD52 and CD70, or engineering the T cells to express a suicide gene that can be triggered in case of GVHD [57,58,59]. Here, CD52 is linked to graft versus host disease.