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Fetal arrhythmias are a common phenomenon of pregnancies. However, debates remain with regard to the etiologies and early treatment of choices for severe fetal arrhythmias. The gene regulatory networks govern cardiac conduction system development to produce distinct nodal and fast conduction phenotypes. The slow conduction properties of nodes that display automaticity are determined by the cardiac ion channel genes, whereas the fast conduction properties are regulated by the transcription factors. Mutations of genes specific for the developmental processes and/or functional status of cardiac conduction system including ion channel promoter (
minK-lacZ
), GATA family of zinc finger proteins (
GATA4
), the homeodomain transcription factor (
Nkx2.5
), the homeodomain-only protein (
Hop
) and the T-box transcription factors (
Tbx2, Tbx3
and
Tbx5
), hyperpolarization-activated cyclic nucleotide-gated channel 4 (
HCN4
) and connexins, may cause fetal arrhythmias. It is expected that development of investigational antiarrhythmic agents based on genetic researches on cardiac conduction system, and clinical application of percutaneously implantable fetal pacemaker for the treatment of fetal arrhythmias would come to true.