TNF and myocardial infarction: Stress-activated protein kinase c-Jun NH2-terminal kinase (SAPK/JNK) is activated by many types of cellular stress and extracellular signals, including UV and y-irradiation, protein synthesis inhibitors (anisomycin), hyperosmolarity, toxins, ischemia/reperfusion injury in heart attacks, heat shock, anticancer drugs (cisplatinum, adriamycin, or etoposide), ceramide, T-cell receptor stimulation, peroxide, and inflammatory cytokines, including TNFα [28].