However, it has become apparent that therapy-induced activation of antiviral signaling can also trigger interleukin-1 (IL-1)-driven antiviral responses, which may not be advantageous as IL-1 promotes the production of cytokines that directly enhance tumor growth or inhibit anti-tumor immunity through the recruitment of myeloid-derived suppressor cells (MDSCs) to the tumor microenvironment (TME) (8). This evidence concerns the gene IL1B and neoplasm.