Recently, Wang et al. reported the critical role of PIWIL1 in mediating the crosstalk of cancer cell metabolism and immune cell response of HCC, and they found that overexpression of PIWIL1 promoted the proliferation rate of human HCC; moreover, they revealed that PIWIL1 increased energy production and oxygen consumption through fatty acid metabolism without altering aerobic glycolysis, and PIWIL1 attracted myeloid-derived suppressor cells (MDSCs) into the tumor microenvironment (TME) and activated p38-MAPK signaling, which in turn improved secretion of immunosuppressive cytokine IL10 [47]. This evidence concerns the gene PIWIL1 and hepatocellular carcinoma.