Dysregulation of the JAK2 signaling pathway promotes cell development and prevents apoptosis in many different hematological malignancies. Further, western blot results proved that Turbo RFP didn’t inhibit the expression of Bcl xL protein in HeLa cells. Accordingly, Turbo RFP did not show obvious toxicity in HeLa cells in three days, and Bcl xL had no impact on growth of cells showing Turbo RFP. We also compared the average fluorescence intensity for cells transfected with DsRed, DsRed Express2, Turbo RFP or GFP at 4-8 and 60 h, and the results showed that cells transfected with Turbo RFP or GFP shown much higher average fluorescence intensity than those of DsRed and DsRed Express2. The protein expression level may be calculated from dividing the common fluorescence intensity by the relative perfection of every protein. As purchase Doxorubicin demonstrated in Supplementary Fig. 3, the expression levels of DsRed Express2, Turbo RFP and GFP are related, and are about 10 times greater than that of DsRed. Considering that DsRed has a lot longer maturation time, even if only 10% of the stated DsRed is matured, its expression level is simply similar to another fluorescent proteins. Thus, the huge difference in cytotoxicity isn’t associated with the expression amount of fluorescent protein. In conclusion, we have shown that DsRed and DsRedExpress2 can prevent the expression of anti apoptotic protein Bcl xL, which results in cytotoxicity in Hela cells. Meanwhile, the expression of Bcl xL inhibits DsRed mediated cytotoxicity. Our results show a mechanism of DsRed cytotoxicity, further investigating the depth mechanism Metastatic carcinoma for DsRed and DsRedExpress2 on inhibition of Bcl xL translation might help to ease the cytotoxic problem of DsRed and its variants. Janus kinase 2 is really a non receptor tyrosine kinase and an essential signal transducer of numerous cytokine signaling, including erythropoietin. Recently, a novel somatic mutation of JAK2, V617F, was determined in neoplasms, including 9-5 polycythemia vera patients and 50-year of patients with essential thrombocythemia and primary myelofibrosis. JAK2 V617F mutant is constitutively angiogenesis cancer causes and active cytokineindependent emergency of JAK2 poor erythroid progenitor cells. In-addition, while in the presence of erythropoietin receptor, JAK2 V617F mutant indicates tumorigenesis in nude mice, suggesting that JAK2 V617F mutant features as a oncogene in the presence of EpoR as a signaling scaffolding. Moreover, JAK2 V617F mutant demonstrated resistance to some DNA cross linking drug, mitomycin C, suggesting that JAK2 V617F mutant initiates emergency signals against apoptosis induced by not only cytokine treatment but also DNA damage.