Furthermore, TAM interactions with CD44+ ovarian CSCs have been shown to promote ovarian cancer recurrence and multidrug resistance (183), and a recent study showed that not only increased STAT3 signaling within TAMs can induce CD44 expression and CSC-like phenotype in ovarian cancer cells, but high CD44-expressing ovarian CSCs are able to further promote the M2 phenotype through STAT3 activation in macrophages as well, forming a positive feed-forward loop of mutual TAM and CSC activation via CD44/STAT3 cooperation that results in ovarian cancer stemness maintenance and chemoresistance (184). This evidence concerns the gene STAT3 and ovarian carcinoma.