In addition, some cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and in-terleukin-6 (IL-6) induced by chronic liver inflammation including hepatitis viral infection and steatohepatitis activate JNK, resulting in a switch in Smad3 signaling from tumor-suppression to oncogenesis [27–30]. The gene discussed is SMAD3; the disease is neoplasm.