We hypothesize that the presence of competing host IL-2 consumer cells (e.g. bystander T cells and Tregs) in immune-competent models contributes to this major difference between the autocrine and paracrine circuits (i.e. paracrine circuits might be more sensitive to competing IL-2 sink cells), a model consistent with more in depth tumor profiling data in later sections of this paper. This evidence concerns the gene IL2 and neoplasm.