Although JNK1 and JNK2 have somewhat different actions on AML, in general, JNKs phosphorylate TFs, such as c-Jun, ATF-2, p53 and Elk-1, which, in turn, regulate the expression of specific genes to mediate cell proliferation, differentiation or apoptosis [59,60] (Figure 1). This evidence concerns the gene JUN and acute myeloid leukemia.