As illustrated in Figure 2, emerging evidence supports the increasing expression of a range of pro-inflammatory cytokines during the course of the disease, including interleukin-15 (IL15) IL32, IL10, and SOCS3. These cytokines have been reported to play a pivotal role in suppressing cell-mediated anti-tumor responses while promoting a chronic pro-tumorigenic inflammatory microenvironment that fuels malignant T-cell proliferation. The gene discussed is IL15; the disease is neoplasm.