Differentiating agents including ATRA, arsenic, cAMP, HDAC inhibitors, and rexinoids relieve this repression through various molecular mechanisms, allowing spontaneous differentiation of leukemic blasts [73].
PML-RAR α has a significant affinity for DR1 [83], a binding site for RXR/PPAR γ heterodimers, and negatively contributes to transactivation by ligand-activated PPRE.