Subsequent development of secondary infection was associated with high constitutive levels of STAT3 pTyr705 in monocytes, CD8+ T cells, and neutrophils, and those of pSer727 in neutrophils, and low levels of IL-6–stimulated pSTAT1 in monocytes and CD4+ and CD8+ T cells, and of E. coli-stimulated pNF-κB in lymphocytes (Fig. 4C). The gene discussed is STAT3; the disease is infection.