The latter finding would clearly fit with the concept that immune checkpoint receptors—such as CTLA-4—are upregulated in T-cell accumulations in the tumor micro-environment, so that a high immune checkpoint expression functions as a surrogate for a high number of T-cell accumulations (i.e., a high T-cell density, an inflamed immune phenotype)21,43–45. Here, CTLA4 is linked to neoplasm.