The prevalence of pediatric obesity has increased over the past 40 years and the rate in females 6 to 19 years old is currently over 19%. This profound increase in obesity is predicted to negatively impact health and result in multiple obesity‐related comorbidities in adulthood. Obesity disproportionately affects ethnic minorities with a higher percentage of adolescent African‐American females (~29%) with obesity compared to non‐Hispanic, white females (~15%). The overconsumption of highly palatable, energy dense, foods are linked to obesity and single nucleotide polymorphisms (SNP) from taste genes are linked to alterations in taste perception and food choices. SNPs are associated with higher rates of obesity and altered fat perception (CD36; fat), higher caloric intake from sugar (TAS1R2; sweet) and increased energy intake (TAS2R38, bitter). An enhanced understanding of genetic, environmental, and behavioral factors contributing to excess weight in adolescents is paramount. Therefore, the goal of the current study was to investigate the intersection of genotype (rs1761667 of CD36 (AA), rs35874116 of TAS1R2 (TT) and rs713598 of TAS2R38 (CC)) and phenotype on diet intake and quality in adolescent African‐American and white females. Genotype was determined by allelic discrimination assay in females (10‐16 years old; n=142) enrolled in the Translational Investigation of Growth and Everyday Routines in Kids (TIGER Kids) Study. Anthropometrics and 24‐hour dietary recalls were conducted for each participant and Healthy Eating Index (HEI) scores, a measure of diet quality, were calculated. The effect of race and genetic variation was assessed using a two‐way ANOVA. Based on allelic discrimination assays, the expression rates of CD36 AA, TAS1R2 TT and TAS2R38 CC in white females (27.7%, 45.0%, 38.3%, respectively) and African‐American females (15.3%, 37.3%, 31.0%, respectively) were determined. Preliminary results indicated that BMI percentiles were higher in African‐American females across all genotypes (p<.05) and moderately affected by TAS2R38 genotype (p<.06). CD36 and race differentially affected HEI for added sugar, total vegetable, greens and beans, whole grain, seafood and plant protein and total HEI, (p<.05). TAS1R2 and race differentially affected HEI‐added sugar (p<.05). TAS2R38 significantly affected HEI‐sodium and total protein (p<.05) and TAS2R38 and race differentially affected HEI for total vegetables, fruits, and whole fruits (p<.09). Fat and sugar intake (g) were positively correlated with SNPs previously associated with altered fat perception (CD36 AA), sugar intake (TAS1R2 TT) and overall energy intake (TAS2R39 CC) in white (p<.05), but not African‐American females, suggesting that the effects of taste receptor SNPs on the relationship between fat and sugar intake differs by race. Overall, the results from these analyses support the intersection between race and genetic variation on HEI, and suggest that SNPs in taste receptor genes differently affect diet quality in adolescent females. Further understanding of the role of taste receptor SNPs on food choices and diet quality is needed to better tailor dietary interventions in the pediatric population.