Barring few differences, neutrophils isolated from B16F10 tumors also showed similar increase in many of the same proinflammatory cytokines and chemokines when treated ex vivo with rmIL-36γ (Supplemental Figure 5D), suggesting that bone marrow neutrophils can be used as a model for tumor-infiltrating neutrophils in investigating the effect of IL-36R signaling on their antitumor responses. The gene discussed is IL1RL2; the disease is neoplasm.