In particular, TNF-α and IL-6 stimulate the compensatory growth of hepatocytes through Nf-κB, mTOR and STAT3 in response to mitochondrial-induced apoptosis and, simultaneously, sustain a pro-survival tumor microenvironment via the paracrine/autocrine release of chemokines (CCL2, CCL7 and CXCL13) and cytokines (IL-1β, IL-6, TNF–α) [116,133,134,135,136]. Here, STAT3 is linked to neoplasm.