Other than the RNase1-mediated cytotoxic effect through RNA degradation, our findings provide information about an additional mechanism by which RNase1 enhances T cell activation in regulating breast tumor shrinkage, likely through the association with EphA4 on T cells in the TME, in which the ligand-receptor interaction is known to be independent of the RNase's ribonucleolytic activity 24, 70. The gene discussed is RNASE1; the disease is breast neoplasm.