It activated proinflammatory responses and relieved immunosuppression of tumor-associated macrophages in the liver cancer cell microenvironment by triggering tumor necrosis factor receptor superfamily member 1 (TNFR1)-mediated NF-κB and p38 MAPK signaling cascades, which subsequently resulted in apoptosis of liver cancer cells (234). This evidence concerns the gene NFKB1 and neoplasm.