In the context of immune checkpoint blockade (ICB) therapy, particularly with anti-PD-1 (programmed cell death protein 1) agents, CD8 + T cells that are unblocked by PD-1 inhibition initiate the PD-L1/NLRP3 inflammasome signaling cascade, which recruits granulocytic myeloid-derived suppressor cells (MDSCs) into the tumor microenvironment, thereby enhancing anti-tumor responses [96]. This evidence concerns the gene CD8A and neoplasm.