STAT3 and neoplasm: TNF-α and IL-6 also promote the compensatory growth of hepatocytes through NF-κB, mTOR, and STAT3 in response to mitochondrial-induced apoptosis and preserve a pro-survival tumor microenvironment via the paracrine/autocrine release of chemokines (CCL2, CCL7, and CXCL13) and cytokines (TNF-α, IL-1β, IL-6) [156].