In case of congenital disease in Polish fetuses and neonates, the participation of the analyzed TLR2 SNP in the development of HCMV infection seems to be fairly plausible through reduced TLR2 activity, impaired heterodimerization of TLR2 with TLR1 molecule, affected TLR2/Myd88 signaling as well as TLR2-dependent NF-κB molecule. The gene discussed is NFKB1; the disease is cytomegalovirus infection.