The protein tyrosine phosphatase SHP-1 dephosphorylates BCR-ABL1, thereby serving as a potential control mechanism of BCR-ABL1 kinase activity. Pathways regulatingSHP-1expression, which could be exploited in the therapeutics of TKI-resistant chronic myeloid leukemia (CML), remain unknown. Moreover, the questions of whether there is any kind ofSHP-1deregulation in CML, contributing to disease initiation or evolution, as well as the question of prognostic significance of SHP-1, have not been definitively answered. This study shows moderately lowerSHP-1mRNA expression in chronic phase CML patients in comparison to healthy individuals and no change inSHP-1mRNA levels after successful TKI treatment. Mutational analysis of the aminoterminal and phosphatase domains of SHP-1 in patients did not reveal genetic lesions. This study also found no correlation ofSHP-1expression at diagnosis with response to treatment, although a trend for lowerSHP-1expression was noted in the very small non-responders’ group of the 3-month therapeutic milestone. [ABSTRACT FROM AUTHOR]