Tumor-associated DCs can induce tumor immune evasion via suppressing the functions of various T cell subsets and NK cells through multiple ligand-receptor pairs, including PD-1/PD-L1, and promoting the expansion of Tregs, which can mediate the loss of HLA-DR from DCs to maintain their tumor immunosuppressive activity, forming a positive feedback loop [13, 15, 16]. The gene discussed is CD274; the disease is neoplasm.