Inhibition of XPO1 by selinexor results in nuclear accumulation and functional reactivation of tumor suppressor proteins such as p53, RB1 (retinoblastoma), and CDKN1B (cyclin-dependent kinase inhibitor 1B); reduces translation of oncogene mRNAs such as Myc, Bcl-2 (B-cell lymphoma), and Bcl-6, and NFκB and activation of multiple pathways leading to apoptosis of cancer cells (54). The gene discussed is MYC; the disease is retinoblastoma.