Azacytidine (5-Aza) is a chemotherapeutic drug that has been known to restore the expression of Tumour suppressor genes by de-methylation and shown clinical efficacy inMyelodysplastic syndrome (MDS) [1-3]. Currently, 5-Aza is being used in UK for the treatment of some adults with MDS, chronic myelocytic leukemia (CML) and acute myelocytic leukemia (AML) [4]. Majority of CML patients treated with imatinib, a BCR/ABL inhibitor would develop resistance under prolonged therapy. Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that is constitutively activated in various human cancers including hematological malignancies. Activation of STAT3 represents an important mechanism of imatinib resistant [5]. Methylation of SHP-1is involved in the constitutive activation of STAT3 [6], and a low level of SHP-1is not sufficient to inhibit activated STAT3 [7]. Epigenetic silencing of SHP-1also plays a role in the development of resistance to imatinib in BCR/ABL positive CML cells.