Thus, functional studies across 3 unique patients, distinct from scRNA-seq or flow cytometry cohorts, validate that KLRG1–E-cadherin interactions can inhibit MHC class II–dependent autologous tumor killing by cytotoxic CD4+ T cells (Figure 7E), in a mechanism that is distinct from and complements PD-1 blockade. This evidence concerns the gene PDCD1 and neoplasm.