HDAC inhibitors are potential novel therapies for the treatment of AML,268 which not only disrupt c-Myc activity but also suppress its expression (Fig. 5a).269 While dimerized with Max, c-Myc resides on the promoter of the pro-apoptotic gene TRAIL and represses its transcription by binding to Miz1 and Sp1 (Fig. 5a). Here, TNFSF10 is linked to acute myeloid leukemia.