Although gastric tumourigenesis in gp130Y757F mice occurred independently of IL6 [32], we found that MyD88-deficiency reduced their tumour burden (Jarnicki A, Puoczki T, Ernst M: A mouse model for innate immune cell-mediated gastric tumorigenesis, submitted), consistent with our observation that excessive Stat3-activation increases Tlr4 expression and susceptibility of these mice to lipopolysaccharide-induced septic shock (Jenkins B, Jarnicki A, Thiem S, Ernst M: Systemic alteration of IL6-mediated Stat3 signaling increases susceptibility to endotoxemia in mice, submitted). This evidence concerns the gene IL6 and serum lipopolysaccharide activity.