Glucose-6-phosphatase dehydrogenase (G6PD) deficiency is the most common enzyme deficiency in humans, affecting 400 million people worldwide and a high prevalence in persons of African, Middle Asian countries. The most common clinical manifestations are neonatal jaundice and acute hemolytic anemia, which is caused by the impairment of erythrocyte’s ability to remove harmful oxidative stress triggered by exogenous agents such as drugs, infection, or fava bean ingestion. Neonatal hyperbilirubinemia caused by glucose-6-phosphate dehydrogenase (G6PD) is strongly associated with mortality and long-term neurodevelopmental impairment. Aim:To determine a level of glucose-6-phosphate dehydrogenase in healthy neonates.The 76.5% of all participants (n=205) was assessed 4.36±1.15 Ug/Hb in normal reference range of G6PD other 23.5% (n=63) was 0.96±0.51 Ug/Hb with G6PD deficiency. In the both sex, 51.5% of male 0.88±0.46Ug/Hb (n=33) and 47.6%of female (n=30) 0.97±0.55Ug/Hb was assessed with G6PDdeficiency. Developing Jaundice period in number of 63 neonates with G6PD deficiency, 85.7% of neonates (n=54)was in 24-72 hours, 4% of neonates (n=3) was in 5-7 days and there is no sign of jaundice in 9% (n=6).Therefore neonates with G6PD deficiency, 53.9% (n=34)contiuned jaundice more than two weeks.G6PD deficiency was determined in male neonates (51.5%) more than female(47.6%). The 76.5% of all participants (n=205) was assessed 4.36±1.15 Ug/Hb in normal reference range of G6PD other 23.5% (n=63) of all participants was 0.96±0.51 Ug/Hb with G6PD deficiency. It shows that G6PD might be one potential risk of neonatal jaundice and hyperbilirubinemia in neonates in Mongolia.