Rackham et al. recently showed that a silver phosphine complex selectively induces apoptosis in transformed Caspase inhibition cells by inhibiting Trx and TrxR. They also confirmed that the delocalised lipophilic cation gathered in the mitochondria. Another recent study employed two dimensional proteomic expression profiling to analyze the action of Flupirtine a gold complex that has been selectively toxic to cancer cells. Interestingly, the authors discovered that among the few proteins with altered expression was Prx3, which showed a 3 fold decrease in expression. Auranofin has been proven to induce apoptosis in cisplatin resistant cancer cells, indicating that anti cancer drugs targeting TrxR might over come some kinds of drug resistance. It’s proposed that TrxR inhibitors are selectively toxic to changed cells because such cells count on increased TrxR activity to maintain DNA synthesis and redox homeostasis. Consistent with this notion, reports using natural gold things similar to auranofin are finding that transformed cells exhibit a larger sensitivity to the drug compared to normal cells. We unearthed that overexpression Retroperitoneal lymph node dissection of the oncogenic protein Bcl 2 successfully blocked auranofin triggered apoptosis. Considering that several cancers overexpress anti apoptotic Bcl 2 family unit members, it is possible that drugs targeting TrxR may encounter similar resistance issues as conventional chemotherapy. As such, it would also be of interest to determine whether small molecule inhibitors of the Bcl 2 family, such as ABT 737, can act synergistically with TrxR inhibitors to promote cancer cell death. Regardless of this possible issue, auranofin was still able to prevent the growth of cells resistant to apoptosis. This really is consistent with recent studies demonstrating that knockdown of TrxR causes a dramatic reduction in tumour progression order Clindamycin in vivo. These results strengthen the theory that TrxR is just a key drug target, as its inhibition might have multiple effects including triggering death in cells with intact apoptotic machinery and inhibiting expansion of apoptosis resistant cells. Until recently auranofin was the primary agent used to treat rheumatoid arthritis. General auranofin is well tolerated at doses of 6 mg/day. However, a group of patients on auranofin may demonstrate undesirable negative effects such as diarrhoea, gastro intestinal upset and skin rash. It remains to be viewed if the strong cytotoxicity of auranofin is responsible for such side effects. In conclusion, we’ve shown that auranofin disturbs mitochondrial redox homeostasis and induces apoptosis via mitochondrial outer membrane permeabilization and apoptotic signalling activities governed by the Bcl 2 family.