In genetically engineered NR2F6-deficient mouse models, the absence of NR2F6 leads to enhanced activity of tumor-infiltrating effector T cells, resulting in increased secretion of IFN-γ and IL-2 and augmented memory function of CD8+T cells, demonstrating superior efficacy compared to PD-1 monotherapy [140]. Here, PDCD1 is linked to neoplasm.