Chimeric antigen receptor (CAR) is a synthetic antigen receptor containing a specific antigen-recognition ectodomain to make T cells selectively attack cancer cells, a hinge-transmembrane region to confer stable surface expression, and one or more intracellular signaling domains to regulate T-cell activation. CAR T-cell therapy has produced unprecedented clinical outcomes for treating cancers, particularly B-cell malignancies. However, increasing clinic data reveal some limitations of current CAR T therapies. For example, >30% of B-cell malignancy patients who initially achieved complete remission encountered relapses after 1-year infusion of CAR T cells. In case of solid tumors, most of the patients did not benefit from CAR T treatment (Park et al., 2018; Schmidts and Maus, 2018). CAR T-cell persistence, defined as how long CAR T cells could survive in vivo after infusion into patients, is one of the major factors affecting the clinical outcomes of CAR T therapy (Porter et al., 2015). Therefore, it is important to understand the molecular mechanism(s) controlling the persistence of CAR T cells.