We have previously shown that Trib2 leukaemogenic potential relies on the ability to promote proteasomal dependent degradation of the tumour suppressor transcription factor CCAAT/enhancer-binding protein α (C/EBPα) and reported elevated TRIB2 expression in a subset of human myeloid leukaemia patients with dysregulated C/EBPα profile and mixed myeloid/T-lymphoid phenotype14,15. The gene discussed is TRIB2; the disease is myeloid leukemia.