However, this phenomenon can be regarded as a sort of vulnerability exploited to restore FoxO signaling with inhibitors of nuclear export, as shown for FoxO1 with the XPO1 inhibitor selinexor in combination with cisplatin in ovarian cancer cells or for FOXO3 with psammaplysene in colon cancer cells [64,65]. The gene discussed is FOXO1; the disease is colonic neoplasm.