Preclinical studies showed that when this protein was relocated to the nucleus by blocking nuclear export with exportin-1 (XPO1) inhibitors, or degraded with proteolysis targeting chimera (PROTAC) therapy, HOX genes were downregulated and cells were able to differentiate, prolonging the survival in an NMP1 mutated AML mouse model [105]. Here, XPO1 is linked to acute myeloid leukemia.