Given that SUV39H1 ablation can concurrently reverse the exhausted state of T cells and that small molecule inhibitors targeting SUV39H1 pharmacologically have equivalent effects with SUV39H1 disruption, the development of corresponding small molecule inhibitors or exploration of combination with SUV39H1‐disrupted CAR‐T cell therapy both affecting the biological behaviors of some specific cancer cells and CAR‐T cells may hold promise as a promising superposition strengthening strategy to conquer solid tumors despite of the possibility that systematic AEs exist. Here, SUV39H1 is linked to cancer.