In particular, p-EMT metastatic cancer-2 cells located at the tumor front exhibited stronger signaling crosstalk with mCAFs than with other mEpCs, mediated by chemokines and growth factors, such as the TIMP1–FGFR2 and HGF–CD44 pairs, and interactions such as those between the EMT-promoting TGF-β –TGF-β receptor, FGF2–FGFR3, and CXCL12–CXCR4 pairs. The gene discussed is FGFR2; the disease is neoplasm.