To explore the mechanism of RPS27a up-regulation in the transition from CML-CP to CML-AP/BP, We hypothesized that some highly expressed proteins (P-gp, AXL, Hsp-70, STAT3, STAT5, CIP2A, BMI-1 and ABCG2) in imatinib resistant CML cells contributed to the up-regulation of RPS27a gene [13–19, 21, 22, 32]. The gene discussed is BMI1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.