BCR-ABL inhibits BGL3 expression via MYC-dependent DNA methylation and loss of BCR-ABL results in the increase of BGL3, decrease of MYC expression and sensitization of leukemia cells towards imatinib-induced apoptosis, suggesting that BGL3 acts as a tumor-suppressor in CML [146]. Here, MYC is linked to chronic myelogenous leukemia, BCR-ABL1 positive.