Considering our outcomes, the common contribution of TLR2 2258 and TLR9 2848 G>A polymorphisms to the development of congenital infection seems to be particularly possible, since TLR9 2848 G>A SNP was also previously reported to be involved in an increased risk of HCMV infection among fetuses and neonates, although the polymorphism is not associated either with amino acid changes of TLR9 molecule or with alterations of the regulatory site of TLR9 gene [14, 52]. The gene discussed is TLR9; the disease is cytomegalovirus infection.