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. The gene discussed is NFATC2; the disease is graft versus host disease.