In the HIC1-deleted breast cancer cells, CXCL14 bound to its novel cognate receptor GPR85 on CAFs in the TME and was responsible for activating these fibroblasts via the extracellular regulated MAP kinase1/2 (ERK1/2), AKT, and neddylation pathways, promoting cancer progression via the induction of the epithelial-mesenchymal transition (EMT) by the CCL17/CCR4 axis [45]. This evidence concerns the gene CCL17 and breast cancer.