Abstract—Chimeric Antigen Receptor (CAR)-T cell therapy has achieved remarkable success in the treatment of hematological malignancies, but its efficacy in solid tumors is still severely limited by T cell exhaustion. As one of the core regulators of T cell exhaustion, Programmed Cell Death Protein 1 (PD-1) plays a key role in this process. However, current targeting strategies for PD-1 still have inherent limitations, making it difficult to strike a balance between effective anti-tumor and maintenance of immune homeostasis. This article proposes a new regulatory strategy that uses PRIME editing technology to precisely modify the PD-1 promoter. As a new generation of gene editing tools, PRIME can achieve precise replacement at the single nucleotide level without inducing DNA double-strand breaks. By precisely modifying key regulatory elements in the PD-1 promoter region, this strategy can moderately downregulate PD-1 expression and effectively alleviate T cell exhaustion while retaining partial PD-1 function to maintain immune homeostasis. This regulatory idea provides a new technical path and theoretical support for the future construction of universal CAR-T cells with low exhaustion and high persistence.