The hypothesis of this study is that SHP-1, a negative regulator gene of JAK/STAT signaling, loses its tumor-suppressive activity in CML due to epigenetic silencing, leading to JAK/STAT signaling hyperactivation, and TQ can re-express this TSG via hypomethylation of the SHP-1 promoter region. This evidence concerns the gene SOAT1 and neoplasm.