Acute promyelocytic leukemia (APL) was clinically defined in the late 1950s as a rare AML subtype, characterized by the expression of PML/RARA, a fusion oncoprotein, which not only impedes granulocyte differentiation by interfering with the nuclear receptor signaling pathways but also disorganizes PML NBs, hence disrupting PML-regulated senescence or apoptosis pathways [149,150,151]. Here, PML is linked to acute myeloid leukemia.