While studies in melanoma and hepatocellular carcinoma suggest that CXCL10 signaling can support a pro-tumor microenvironment dominated by MDSC and macrophages [74,123], findings in early-stage pancreatic cancer indicate a protective role, where CXCL10 was essential for recruiting and maintaining an anti-tumor M1 macrophage population, and its absence caused a shift toward a pro-tumoral M2 phenotype that promotes angiogenesis, tissue remodeling, and metastasis [25]. The gene discussed is CXCL10; the disease is familial pancreatic carcinoma.