Chronic myeloid leukemia (CML) epitomises successful targeted therapy with 90% patients in chronic phase treated with tyrosine kinase inhibitor (TKI) attaining remission. This success eludes 80% patients in advanced blast crisis (BC) resistant to TKIs due to either kinase domain mutations in the transforming protein Bcr/Abl preventing TKI binding or progression of leukemic cells to Bcr/Abl independent phenotype wherein alternate signalling pathways drive the disease. This brings in a need to identify alternate therapeutic targets for TKI resistant CML-BC. Present study aims at achieving this through delineating Bcr/Abl downstream and alternate signalling pathways by labelled and label-free quantitative proteomic analysis of sensitive and resistant CML-BC cell lines.