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Aim: Epithelial sodium channels play an important role in the regulation of movement of sodium and absorption of alveolar fluid during prenatal period. Transient tachypnea of the newborn is a common respiratory problem in term or near-term infants. A lack of maturation of epithelial sodium channels is considered in its etiology. However, the role of genetic factors is unclear. The purpose of this study is to determine the role of gene SCNN1A which is responsible for synthesis of epithelial sodium channel alpha unit which is known to be effective in the mechanism of the disorder. Material and Method: Newborn infants>37 weeks of gestation with a diagnosis of transient tachypnea of the newborn followed up at Neonatal Intensive Care Unit of Akdeniz University Medical Faculty between July 2010 - January 2012 and a control group consisting of healthy infants at the same gestational age were included in the study. 2 cc of blood with EDTA was obtained from both groups in the first five days of their life and blood samples were kept at -80° degree. DNA isolation was fulfilled in the Department of Medical Biology. The gene was displayed using BigDye Terminator with the method of Sanger sequencing. The study was approved by the ethics committee (B.30.2.AKD.0.20.05.05). Results: Both the transient tachypnea of the newborn group and the control group were consisted of 32 infants. Through the sequence display method, all the exons of the SCNN1A gene which codes the alpha subunit of epithelial sodium channels were displayed. Nevertheless, no significant change was found. Conclusions: In conclusion, no relationship was established between the development of transient tachypnea of the newborn and the SCNN1A gene which is responsible for the synthesis of alpha subunit of epithelial sodium channels. However, this preliminary study is considered to be a threshold for an extended research with a wider range of patients to obtain more precise results. [ABSTRACT FROM AUTHOR]