Mixtures of CXCL4 and CXCL12 or obligate CXCL4•CXCL12 heterodimers inhibited CXCL12-induced migration of breast MDA-MB-231 cancer cells, increased Ca2+ release and activated downstream signaling of CXCR4 but not of CXCR3, highlighting its role in the limitation of cancer progression [76,77]. This evidence concerns the gene CXCR3 and cancer.