As shown in Figure 10, this study addressed a reasonable mechanism that BM microenvironment protected CML-LSC cells from IM-induced cell death through BCR/ABL-independent activation of Stat5, consequently upregulated the DNA binding activity of NF-κB though binding of p-Stat5 and p-RelA, and resulted in RelA acetylation in nucleus. The gene discussed is STAT5A; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.