CCL5 and neoplasm: GBE1 blockade promotes the secretion of CCL5 and CXCL10 to recruit CD8+ T lymphocytes to the tumor microenvironment via the IFN-I/STING signaling pathway, accompanied by upregulation of PD-L1 in lung adenocarcinoma cells; this indicates that GBE1 is a promising cancer immunotherapy target for achieving tumor regression in lung adenocarcinomas [54].