Our study demonstrated that ADORA2A-AS1 is upregulated in CML, and knockdown of ADORA2A-AS1 inhibits cell proliferation, induces cell apoptosis and cell cycle arrest, and enhances imatinib-induce apoptosis through regulating miR-665, with TGFBR1 and ABCC2 as its downstream effectors. This evidence concerns the gene ABCC2 and chronic myelogenous leukemia, BCR-ABL1 positive.