ULBP2 and pancreatic adenocarcinoma: On the other hand, TP53, as the second mutated factor in the PAAD genome, plays a non-negligible role in promoting PAAD invasion, PD-L1 kinetics, and immune evasion (15).TP53 mutations can not only inhibit innate immune responses through tumor-associated macrophages and neutrophil surface toll-like receptors but also reduce ULBP1- and ULBP2-mediated anti-tumor activity of NK cells and affect the number of T cell infiltrates through dendritic cells (37, 38).