As a result, the downstream effectors including PIK3/Akt, MAPK and p-STAT5 were repressed and in vitro and in vivo growth of both imatinib-sensitive and resistant CML cells, i.e., BCR-ABL-harboring K562 and BCR-ABL T315I-harboring K562R were inhibited. The gene discussed is AKT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.