The current view, derived from gene expression studies across multiple human cancers suggests that the inflammatory phenotype typified by the expression of Th1 transcripts (i.e. CXCL9, CXCL10, CXCL11 and CCL5) and IFN-stimulated transcripts is also characterized by the counter-activation of suppressive mechanisms (e.g. IDO and PDL1)12, 22, 23. The gene discussed is CXCL10; the disease is cancer.