One other study recently described a HIF-1α dependent accumulation of MDSC under tumor conditions; in a mouse model of hepatocellular carcinoma, HIF-1α activation in tumor cells led to an overexpression of the ectonucleotidase CD39 mediating a differentiation arrest of MDSC thereby leading to their accumulation (27). The gene discussed is HIF1A; the disease is hepatocellular carcinoma.