Background– G6PD deficiency is one of the important causes of pathological jaundice in neonates. Undetected neonates can land up with increased morbidity ( kernicterus, exchange transfusion etc) and morbidity. Universal Screening in neonates for G6PD deficiency is still not established in India. Aims and objectives– a) Ascertain different causes of neonatal jaundice in our institution requiring therapeutic interventions. b) Estimating the prevalence of Glucose–6–phosphate dehydrogenase deficiency in neonatal jaundice patients of West Bengal, India. c) To find the relation between Glucose–6–phosphate dehydrogenase level and degree of jaundice in the patients. d) Determining the importance of routine neonatal screening for G6PD in newborns born in this geographical area. Patient and method– A cross–sectional study was done on 242 neonates admitted with hyperbilirubinemia (bilirubin >15mg/dl) in baby nursery , Department of Pediatrics, R.G.Kar Medical College & hospital Kolkata, from December 2010 to October 2011 . Only the neonates with congenital abnormalities were excluded from the study. Different parameters that were studied included: i. Detailed history. ii. Physical examination. iii. Complete hemogram. iv. C reactive protein. v. Total and conjugated bilirubin. vi. Direct Coomb’s test vii. ABO and Rh group of mother and baby. viii. Glucose–6–phosphate Dehydrogenase quantative assay. Results– ABO incompatibility was found to be the most common cause of neonatal hyperbilirubinemia. G6PD deficiency was found in 6.61% (16 out of 242 neonates studied). The sex distribution was male 10(81.25%) and female 6 (18.75%). G6PD deficiency was found to be of mild degree(3.84–6.4U/gm Hb) in 37.5% of cases, moderate(0.64–3.84U/gm Hb) in 62.5% cases whereas no case was found to be having severe degree(<0.64U/gmHb) of G6PD deficiency. Total serum bilirubin level in G6PD deficient group was found to be significantly higher (p<0.05) than blood group incompatibility group or other causes of pathological jaundice combined. Requirement of Exchange transfusion as well as prolonged Phototherapy was significantly higher (p value<0.05) in G6PD deficient neonates than due to any other causes. Neither Sex nor any clinical nor any routine biochemical parameters were found to be of any predictive value for detection of G6PD deficiency in neonates. G6pd level of neonates with gestational age 30–32 weeks were found to be significantly higher than neonates with gestational age 38–40weeks and 40–42weeks (pvalue <0.05) Conclusion and recommendations– G6PD is one of the leading cause of Hyperbilirubinemia (Bilirubin>15mg/dl) in neonates. They usually present with very high bilirubin level requiring exchange transfusion or prolonged phototherapy or both adding to their morbidity and mortality. No clinical or routine biochemical predictors are available to detect G6PD deficiecy. Preterm babies < 32 weeks gestation may show higher G6PD level initially after birth thus level may be repeated later if suspicion of deficiency is there. G6PD level screening is available in every laboratory. As undetected G6PD deficiency carries a high morbidity– mortality and thus medicolegal implications. This study recommends routine newborn screening for G6PD deficiency in every neonatal units in India. We have started routine screening in our unit and requirement of exchange transfusion in our unit is on the decrease.