Thus, the first approach to impacting CRM1-dependent cancers was full inhibition of the protein with the use of the irreversible CRM1 inhibitor Leptomycin B; however, it was quickly determined that too much inhibition leads to death of non-malignant cells due to mislocalization of critical cellular proteins and increased nuclear concentrations of pro-apoptotic proteins. The gene discussed is XPO1; the disease is cancer.