More important, we were able to detect phosphorylated STAT1 in VSMCs and ECs of human atherosclerotic plaques (Fig. 6), which correlated with elevated expression of the chemokines CXCL9 and CXCL10. Recently, Agrawal et al. [10] showed that STAT1 deficiency reduced foam cell formation in an intraperitoneal inflammation model and reduced atherosclerosis in an atherosclerosis-susceptible bone marrow transplantation mouse model. The gene discussed is CXCL9; the disease is atherosclerosis.