Introduction: We aimed to evaluate the candidate genetic variations and maternal diet pattern as risk factors of development of FA. Methods: A total of 1811 infants from the Cohort for Childhood Origin of Asthma and Allergic Diseases (COCOA) birth cohort were available. Infants’ cord blood was genotyped for 11 single nucleotide polymorphisms (SNPs) which had been reported as risk SNPs for allergic diseases and 3 copy numbder variations (CNVs) for a phase II detoxification superfamily. Among 1811 infants, 1635 mothers of them were assessed dietary intakes at 26 weeks pregnant by a food frequency questionnaire and grouped according to five dietary patterns such as “traditional”, “confectionery”, “meat”, “processed”, and “coffee and milk”. FA was defined according to the questionnaires and physician interview in allergy clinics. Result: Among 1811 infants, 162 (8.9%) were diagnosed with FA. The TT homozygote of rs7216389 (odd ratio [OR]=2.265, p=0.002) in human gasdermin-B (GSDMB) and the TT homozygote of rs6265 (OR=1.617, p=0.013) in brain-derived neurotrophic factor (BDNF) were associated with more FA in infants. The C allele of both rs7216389 and rs6265 showed a protective effect for development of FA. The confectionery diet pattern during pregnancy was associated with more FA (OR=1.693, p=0.008). In nutrients analysis according to dietary pattern, the mothers with confectionery diet pattern had a tendency to have more trans-fatty acid (r=0.484, p0.001, adjusting calories and maternal ages). While this effect of maternal diet was preserved in infants without the protective C allele in GSDMB and BDNF, this effect was not shown in those with the C allele. Combining maternal confectionery diet pattern with CNVs of glutathione S-transferase (GST), there were more associations with incidence of FA (OR=1.771 in GSTP1, OR=1.795 in GSTM1, OR=1.927 in GSTT1, all p values 0.05). Conclusion: The interaction between maternal dietary pattern during pregnancy and genetic variations including GSDMB, BDNF and GST can affect the development of food allergy in offspring. Our data would be added to the evidence of gene-environment interaction. This research was supported by the fund (2008-E33030-00, 2009-E33033-00, 2011-E33021-00, 2012-E33012-00, 2013-E51003-00, 2014-E51004-00, 2014-E51004-01) by Research of Korea Centers for Disease Control and Prevention.