Therefore, damaging the MECs layer resulted in the release of various factors (such as SDF1/CXCL12, CXCL14, MMP, and tenascin) [11, 12] with a potential to modify the tumour microenvironment and facilitate the paracrine communication between the tumour epithelial cells and the enclosed stroma enhancing the tumour aggressiveness [11, 13]. This evidence concerns the gene CXCL14 and neoplasm.