Compelling data from Karen Keeshan and Warren Pear [24] also revealed that TRIB2 contains separate binding sites for COP1 and its protein substrate, CCAAT/enhancer protein-α, and that deletion of the COP1 binding site abrogated TRIB2′s ability to degrade this transcription factor, block granulocytic differentiation and induce acute myelogenous leukaemia. Here, COP1 is linked to acute myeloid leukemia.