Similarly, circulating CXCL10 was lower in the prf1−/− cxcl9−/− group (Fig. 3c) suggesting that the lack of effect of CXCL9 deficiency on HLH was not due to compensation by CXCL10, and that like IFN-γ and sIL2r, CXCL10 is in part regulated by CXCL9 itself. Here, IFNG is linked to hemophagocytic syndrome.