TNFRSF4 and neoplasm: We performed a differential analysis of immune-related genes and discovered that the expression levels of LAIR1, an inhibitory immune checkpoint molecule that suppresses T-cell activation by binding to collagen in the tumor microenvironment (27), and TNFRSF4, a co-stimulatory receptor critical for sustaining CD4+/CD8+ T-cell survival and effector function (28), were significantly higher in the high PS group (***P < 0.001).