CXCL10 and cancer: These genetic alterations activate, in a RAS-BRAF-MAPK-dependent manner, transcription of proinflammatory molecules like VEGF-A, CXCL1/GRO-α, CXCL10/IP-10, and CXCL8/IL-8, which can act autocrinously or paracrinously to support cancer cell growth and survival [37,38].