Specifically, they found that TAMs secreted increased amounts of IL-1β under moderate hypoxic conditions, due to the increased stability of HIF-1α, and that the necrotic debris of HCC cells increased IL-1β release by TAMs with an M2 phenotype, via TLR4/TRIF/NF-κB signaling [85]. The gene discussed is IL1B; the disease is hepatocellular carcinoma.