The functional consequences of impaired TLR2 signaling on CMV infection have been established in vivo in both humans and mice: in humans, the most frequent single nucleotide polymorphism (SNP) occurring in TLR2, R753Q [11], is a risk factor for HCMV disease in liver transplant recipients [9,12]; The R753Q mutation was shown to impair tyrosine phosphorylation, dimerization with TLR6, and recruitment of Mal and MyD88, resulting in a functional defect of TLR2 stimulation [10,13]. Here, MAL is linked to cytomegalovirus infection.