Recently, in-depth research has revealed a possible suppressive mechanism by which CAFs in the TME might function in a similar manner to normal DCs, including participating in antigen sampling, processing and presentation and upregulating the expression of immune checkpoint molecules (factor associated suicide (FAS)/factor associated suicide ligand (FASL) and PD-1/programmed death ligand 2 (PD-L2)), thereby promoting a decrease in the number of CD8 + T cells and an increase in tumor cell viability [93]. The gene discussed is PDCD1LG2; the disease is neoplasm.