Anisomycin is a potent protein synthesis inhibitor which interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system^[1]. Anisomycin is a JNK activator, which increases phospho-JNK^[2][3]. Anisomycin is a bacterial antibiotic isolated from Streptomyces griseolus^[4]. IC50 & Target: DNA synthesis^[1] In Vitro: To examine whether JNK has a core role in colistin-induced neurotoxicity in PC-12 cells, an SP600125 (a highly selective inhibitor of JNK) and Anisomycin (a potent activator) are used in this study. In order to select an appropriate concentration, PC-12 cells are treated with a range of SP600125 (0-80 μM) and Anisomycin (0-20 μM) respectively for 24 h. The results show that the cells viability significantly decreases by SP600125 treatment in a concentration-dependent manner, observed at the concentrations greater than 20 μM (p<0.01). Similarly the cells viability is inhibited by Anisomycin treatment (≥8 μM) (p<0.05) ^[1]. In Vivo: Disruption of TNFRp55/p75 attenuates Anisomycin-induced ventricular functional improvements. Anisomycin results in an improvement in left ventricular developed pressure (LVDP), which disappears in animals with disruption of TNFR p55/p75. In addition, the Anisomycin-induced improvement in LVEDP in wild-type animals is eliminated by deletion of TNFR p55/p75. Likewise, disruption of TNFR p55/p75 abrogates the recovery of rate pressure product (RPP) elicited by pretreatment of Anisomycin. TNFR p55/p75^-/- mice without Anisomycin treatment do not show differences in cardiac functional recovery compared with the control wild-type mice. There are no significant differences in heart rate between wild-type and TNFR p55/p75-deficient mice. To see whether Nox2 is involved in Anisomycin-induced myocardial protection, Nox2-deficient mice are treated with Anisomycin. The improvement in the LVEDP in Anisomycin-treated mice is eliminated in Nox2^-/- mice compared with wild-type mice. In addition, recovery of RPP in wild-type mice treated with Anisomycin is mitigated in Nox2^-/- mice. Nox2^-/- mice without Anisomycin treatment do not show the difference in cardiac functional recovery compared with wild-type control mice^[2].