Earl et al (2009) reported that silencing of TLR4 in tumour cells reduces the metastatic tumour burden in steatotic livers. Recently, Killeen et al (2009) suggested that bacterial endotoxins directly promote tumour cell adhesion and invasion through upregulation of urokinase plasminogen activator and the urokinase plasminogen activator receptor through TLR-4-dependent activation of NF-κB. Our study showed that TLR4/MyD88 overexpression was frequently detected in CRC with liver metastasis, and TLR4/MyD88 levels were significantly higher in these CRCs. Here, MYD88 is linked to neoplasm.