Immunoblot examination showed that neither imatinib nor nilotinib removed the phosphorylation of Crkl in the initiation of treatment, but dasatinib did. To evaluate if the RIs correlate with the medical response to TKIs, newly diagnosed patients were divided in-to two groups in accordance with the newest result, imatinibsensitive, who achieved an optimal response dub assay after the sample collection, and imatinib immune, who did not. The RI of the people within the group was 4. A day later and that in the resistant group was 43. A day later. We also considered the predictability of the response to nilotinib. Eight people imatinib resistant had undergone nilotinib therapy. Included in this, 4 reached optimal responses and the others failed. The mean RI in the nilotinib vulnerable group was 3. Five full minutes as opposed to 3-1. 2% in the group. The RIs were obviously divided between dasatinib resistant and sensitive and painful groups, even though sample size was too small to perform statistical analysis. Expected values and the specificities, sensitivities were all hundreds of in terms of dasatinib and nilotinib responsiveness, If the stop value of RI was established at 10%. Also, in the examination of imatinib therapy, the uniqueness and sensitiveness were over 778. Consequently, Skin infection it’s suggested that the RIs are of good use as a novel predictor for clinical application of TKIs, specially in imatinib resistant cases. Imatinib, the very first authorized TKI for CML, generally causes durable cytogenetic remission and hence occupies a crucial position while the present standard of care. Now, second generation TKIs, for example dasatinib and nilotinib, have now been provided. Though these TKIs are significantly more powerful and show greater sensitivity against some imatinibresistant mutations, there are no useful instructions for the proper range of second generation TKIs in resistant individuals. More over, second-generation TKIs have already been recommended supplier Capecitabine as first-line treatments based on the evidence an earlier achievement of remission may provide a better clinical outcome or less illness progression. There’s still a need for signals pointing to the proper drug choice for individual patients. The IC50, a mobile based screen for resistance determining the drug concentration that could induce 5000-6000 of growth reduction, is a powerful predictor of the responsiveness to drugs. In-patients with de novo CML, the IC50imatinib was reported to obtain a top predictive value. But, dedication of the IC50 for each TKI involves so much work and time that the program suitable for all patients could be a significant remote possibility. Moreover, since the optimal concentration ranges for each TKI, comparing the efficiency between different TKIs is hard.