For example, it binds to the PD-L1 receptor, a well-known immune checkpoint that promotes tumor immune escape; it also causes depletion of T cells and enrichment of depleted CD8+ in the tumor microenvironment; and it induces epithelial-mesenchymal transition (EMT) characteristics of CRC both in vitro and in vivo models [49]. Here, CD8A is linked to neoplasm.