Although, the overall affinity range of the TCRs responsible for GVHD and GVT has not been extensively compared, genetic knockout of several molecules related to TCR signaling, such as NFAT1/2, PKCα, and PKCθ, ameliorated GVHD but not GVT activity, suggesting that GVT responses might be driven by more avid interactions than those in GVHD in general45–47. Here, PRRT2 is linked to graft versus host disease.