Using scRNA-seq, we determined that the combination of PD-1 inhibitor and SMI induced cytotoxic NK cells to infiltrate the NSCLC tumor, recruited DCs to tumors via NK cell activation, alleviated the exhausted state of T and NK cells, reduced angiogenic characteristics in the TME, and diminished cancer metabolism reprogramming-associated CAFs. This evidence concerns the gene PDCD1 and cancer.