Lower expression of JMJD1B in AML patients indicated worse prognosis,42,43 and JMJD1B was thus viewed as a tumor suppressor for AML.44 The underlying mechanism may be the JMJD1B-facilitated degradation of PML/RARα, a critical event in the pathogenesis of acute promyelocytic leukemia (APL).43 JMJD1B also appears as a tumor suppressor in CRC, the histone methylation of which is regulated by PRL-3, an essential metastasis gene of CRC.45 This evidence concerns the gene KDM3B and neoplasm.