T cell TET2 disruption cuts the breaks on antitumor CAR T cell therapy.

Functional persistence of chimeric antigen receptor (CAR) T cells is required for sustaining an antitumor response. Recently, Jain et al. revealed that disruption of TET2 in CAR T cells resulted in antigen-independent CAR T cell hyperproliferation that enhanced tumor control in mice, highlighting the potential of epigenetic strategies to improve T cell-based cancer immunotherapy.