“…Additional genomic alterations, which are involved in cell cycle, DNA damage, signal transduction, and apoptosis (2,3), are also found to contribute to MCL progression and Abbrevations: MCL, Mantle cell lymphoma; GPER, G-protein-coupled estrogen receptor; BTK, Bruton's tyrosine kinase; EGFR, epidermal growth factor receptor; ROS, reactive oxygen species; g-H2A.X, phospho-H2A.X; NOX, NADPH oxidase; NF-kB, nuclear factor kappa-B; NAC, N-Acetyl-L-cysteine; H2DCFDA, 2′,7′-dichlorofluorescin diacetate; DSB, doublestrand break. resistance to conventional chemotherapy (4,5). Recent advances in cytostatic drugs, including the development of immunomodulatory imide drugs such as lenalidomide and the Bruton's tyrosine kinase (BTK) inhibitor such as ibrutinib, have established chemo-free regimes as a promising new direction of MCL therapy (5)(6)(7).…”