These data are consistent with observations in murine pre-clinical models and human tumors wherein upregulation of inhibitory immune checkpoint molecule expression on CD8 + tumor-infiltrating lymphocytes (TILs) is a critical mechanism by which cancer cells can escape the antitumor immune response37–39 Moreover, these data also suggest that, like human cancer patients, high T-cell infiltration of canine soft tissue sarcoma tumors as a determinant of probability of clinical response to cancer immunotherapies warrants further investigation40,41. The gene discussed is CD8A; the disease is neoplasm.