-increased apoptosis/autophagy through mitochondrial dysfunction, ROS, Ca2+, NGF receptor, Fas receptor, caspase-7, cyclins, p21, p53-modification of signaling pathways such as JNK/c-Jun, PI3K/AKT/mTOR, NK-κB, AMPK-antiproliferative effects that regulate tumor growth and metastasis through cell cycle regulators, inhibition of MMP-9, VEGF, Eag1 channels, inhibition of FoxM1-associated DNA repairing, enhanced Lin-7 C expression-inhibition of tumor development by the immune response through cytokines such as TNF, IL-12, IFN, and chemokines. The gene discussed is JUN; the disease is neoplasm.