JUN and acute myeloid leukemia: Poor-risk AML phenotypes, including Flt3ITD+ve, also express transcriptionally-active phospho-c-jun, affecting distinct gene activation.[13-18] C-jun acts with Stat5, in activation of transcriptional targets PIM1, relB, and MEIS1 (a prognostic gene functioning in leukemic stem cells).[15, 17, 18] Further, c-jun and β-catenin, reciprocally and cooperatively, bind the others promoter consensus, thus conveying cooperative transactivation, involving TCF4 elements such as regulate HOXAs.[11, 19, 20]