Upregulation of lncRNA-BGL3 occurs in K562 cells after disruption of Bcr-Abl expression and in primary CML cells derived from patients in response to imatinib treatment; lncRNA-BGL3 functions as a competitive endogenous RNA (ceRNA) to cross-regulate the expression of phosphatase and tensin homolog (PTEN), thereby modulating leukemic cell survival [18]. This evidence concerns the gene PTEN and chronic myelogenous leukemia, BCR-ABL1 positive.