For example, ovarian cancer‐derived exosomal circGLIS3 drives M2 polarization through dual mechanisms: it sponges miR‐1343‐3p to relieve its suppression of PGK1 (phosphoglycerate kinase 1), enhancing glycolytic metabolism, while directly binding vimentin to inhibit its phosphorylation, thereby blocking vimentin‐STAT3 complex dissociation and facilitating STAT3 nuclear translocation [139]. This evidence concerns the gene STAT3 and ovarian cancer.