Mechanistically, tRF5-GlyGCC can interact with KDM6B to epigenetically upregulate Runx2 and transcriptionally activate ITGBL1 and S100A9 expression in HCC cells, which further reduces NK cell cytotoxicity directly and attracts myeloid-derived suppressor cells (MDSC) to inhibit NK cell function indirectly, respectively [24, 25]. This evidence concerns the gene RUNX2 and hepatocellular carcinoma.