Indeed, in vitro studies have shown a reciprocal relationship between primary human prostate cancer CAFs and inflammatory macrophages, whereby CAFs can stimulate monocyte recruitment and promote an M2 macrophage-like phenotype via CAF-derived secretion of CXCL12, and M2-like macrophages were able to elicit activation of normal human prostate fibroblasts via upregulation of αSMA [247]. This evidence concerns the gene ACTA1 and prostate carcinoma.