Julia A. Belk et al. demonstrated through gene editing that ARID1A improves T-cell persistence and that anti-ARID1A deficiency promotes mutability and potentiates therapeutic antitumor immunity, unleashing tumor immunity in vivo [43]; however, deletion of ARID1A gene function and decreased T-cell persistence may be barriers to immune checkpoint blockade and the effectiveness of CAR-T cell immunotherapy [44]. The gene discussed is ARID1A; the disease is neoplasm.