In bone marrow samples from CML patients, the expression levels of HULC correlated positively with MYC and knockdown of HULC retarded the proliferation of CML leukemic cells and induced apoptosis by repressing MYC, Bcl-2 and by upregulating the PI3K/AKT signaling pathway (141). Here, BCL2 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.