Selinexor selectively inhibits XPO1 by forming a slowly reversible covalent bond with cysteine 528 in the cargo binding pocket of XPO1.[7] Selective inhibition of nuclear export by selinexor results in accumulation of tumor suppressor proteins in the nucleus, decreased levels of oncoproteins, cell cycle arrest, and apoptosis of cancer cells, while sparing normal cells.[5–7] Selinexor has been shown to be effective in many clinical trials of AML. The gene discussed is XPO1; the disease is acute myeloid leukemia.