To rule out the possibility that spontaneous tumor control was due to off-target effects from CRISPR/Cas9 mutagenesis, we retrovirally reintroduced IFNγR2 or Jak1 into IFNγR2- and Jak1-mutant cells, respectively, and confirmed successful IFN-γ signaling by upregulation of H-2Kb after IFN-γ stimulation in vitro (Fig. 2b, c). Here, JAK1 is linked to neoplasm.