The present study demonstrated that overexpression of ATF3 or PER2 promotes cuproptosis in OSCC cells by upregulating expression of cuproptosis-related genes DLAT, PDHB, and SLC31A1. Other recent findings have shown that DLAT has a pivotal role in cuproptosis, moreover, regulates PD-L1 expression and enhances the infiltration of tumor-associated macrophages and regulatory T cells [35–38], suggesting a synergistic effect between cuproptosis and tumor immunotherapy. This evidence concerns the gene ATF3 and neoplasm.