IL1B and neoplasm: In the tumor microenvironment release of danger-associated molecular patterns (e.g., HMGB1, HSPs), IL-1β and TNF-α lead to NF-κB activation and translocation of the p65/p50 heterodimer to the nucleus which favors M1 polarization of macrophages although accumulation of the p50 inhibitory homodimer mediates defective responsiveness of TAMs and M2 polarization, associated with inhibition of proinflammatory mediators [77, 78].