Reciprocally, MDSCs contribute to the stemness and survival of cancer cells via multiple mechanisms including (i) the modulation of RNA interference such as upregulation of piRNA-823 to induce NANOG, OCT4, and SOX2 expression [29], (ii) the epigenetic regulation such as secretion of exosomal S100A9 to enhance STAT3/NF-κB phosphorylation which promotes the stemness of cancer cells [30], and (iii) the production of tumor-supportive simulators such prostaglandin E2 (PEG-E2) which expand the ALDH+ CSCs population in uterine cervical cancer [31]. This evidence concerns the gene LDHA and cancer.