In conclusion, these studies suggest that the presence of liver inflammation in the context of DM, leads to the exposure of hepatocytes to increased levels of IL-6 and TNF-α, which promote the activation of JAK/STAT-3 and IKKα/NF-kβ signaling pathways, followed by lack of apoptosis, and consequently uncontrolled proliferation of hepatocytes; this results in initiation and promotion of HCC development [53]. This evidence concerns the gene IL6 and diabetes mellitus.