We hypothesized that: (1) B7H3/Dox@GNCs could selectively target B7H3 positive tumor cells, tumor vasculature, and tumor-associated stromal cells; (2) high stability and long retention in circulation and in situ drug release of Dox would respond to an acidic environment and esterase in tumor cells; (3) NIR-exposure could accelerate drug release and achieve precise spatial–temporal synchronization of chemotherapy/photothermal therapy with low side effects against NSCLC. This evidence concerns the gene CD276 and neoplasm.