Considering the previous data on the function of TLR2 and its 2258 G>A polymorphism, in the related signaling pathways, as well as the outcomes of our study, we suggest that, in Polish fetuses and newborns with congenital HCMV infection, GA heterozygotic status in the analyzed region may cause hypo-responsiveness of the produced TLR2 molecule to infection with HCMV. Here, TLR2 is linked to cytomegalovirus infection.