Dysregulation of the JAK2 signaling pathway promotes cell growth and prevents apoptosis in many different hematological malignancies. Further, western blot results confirmed that Turbo RFP did not inhibit the expression of Bcl xL protein in HeLa cells. Appropriately, Turbo RFP didn’t show obvious poisoning in HeLa cells in three times, and Bcl xL had no influence 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 48 and 60 h, and the results confirmed that cells transfected with Turbo RFP or GFP found greater average fluorescence intensity than those of DsRed and DsRed Express2. The protein expression level may be estimated from dividing the average fluorescence intensity by the relative perfection of every fluorescent protein. As Ivacaftor structure demonstrated in Supplementary Fig. 3, the expression degrees of DsRed Express2, Turbo RFP and GFP are identical, and are about 10 times greater than that of DsRed. Given that DsRed has a lot longer maturation time, even when only hundreds of the expressed DsRed is matured, its expression level is simply comparable to the other fluorescent proteins. Consequently, the huge difference in cytotoxicity isn’t linked to the expression degree of fluorescent protein. In summary, we have demonstrated that DsRedExpress2 and DsRed may prevent the expression of anti apoptotic protein Bcl xL, which leads to cytotoxicity in Hela cells. Meanwhile, the expression of Bcl xL inhibits DsRed mediated cytotoxicity. Our results show a mechanism of DsRed cytotoxicity, further analyzing the depth mechanism Ribonucleic acid (RNA) for DsRed and DsRedExpress2 on inhibition of Bcl xL translation can help to alleviate the cytotoxic problem of DsRed and its variations. Janus kinase 2 is really a non receptor tyrosine kinase and a vital signal transducer of various cytokine signaling, including erythropoietin. Recently, a new somatic mutation of JAK2, V617F, was identified in myeloproliferative neoplasms, including 9-5 polycythemia vera patients and 500-1000 of patients with crucial thrombocythemia and primary myelofibrosis. JAK2 V617F mutant is constitutively CTEP triggers and active cytokineindependent success of JAK2 deficient erythroid progenitor cells. Furthermore, while in the presence of erythropoietin receptor, JAK2 V617F mutant exhibits tumorigenesis in nude mice, suggesting scaffolding as that JAK2 V617F mutant functions as a oncogene in the presence of EpoR. More over, JAK2 V617F mutant displayed resistance to a DNA cross linking drug, mitomycin C, suggesting that JAK2 V617F mutant activates emergency signs against apoptosis induced by not just cytokine elimination but also DNA damage.