Prenatal Alcohol Exposure (PAE) is a leading cause of cognitive disabilities known as Fetal Alcohol Spectrum Disorders (FASD). Interventions that ameliorate PAE’s impact are a high priority. One such intervention is the micronutrient choline, a one-carbon (1C) donor essential for healthy brain development; choline improves cognitive outcomes in both FASD and its preclinical models. However, its benefits are not always clear, and an important modulator of these responses are the known polymorphisms in choline- and 1C-metabolizing genes that affect the metabolism, transport, and utilization of choline and its methyl groups and thus choline needs. We recently reported that for one such gene, the choline transporter SLC44A1, minor alleles known to increase choline needs are associated with greater memory improvement in alcohol-exposed children who received supplemental choline; that is, those who carry the effect alleles have a higher choline need that is met by the supplement. Moreover, in a separate study of control and alcohol-exposed children who never received choline supplements, those same alleles are again associated with greater cognitive impairment, indicating that alleles that increase choline needs also increase the vulnerability to PAE, likely because their greater needs went unmet by current dietary practice. Here, we further explore the choline genetic landscape of those with PAE to identify additional choline-related polymorphisms that modulate cognition and behavior. Specifically, we hypothesize that select polymorphisms in additional genes that affect choline needs significantly influence behavioral outcomes in FASD. Aim 1 tests the hypothesis that there exist polymorphisms in additional choline-related genes that influence behavioral outcomes in those with PAE who consume normal dietary choline (Gene x Exposure). This aim utilizes an existing dataset from those with PAE who were deeply genotyped and phenotyped with respect to neurobehavior. Aim 2 directly tests the influence of a strong candidate gene identified in our preliminary data, ALDH1L1, on cognition and behavior. ALDH1L1 controls the size of choline-derived 1C pools and therefore choline levels. Using an established haploinsufficient mouse model, we will establish 1L1’s role in affecting behavior and vulnerability to PAE. These findings (i) provide novel insight into how alleles affecting choline needs impact behavior in any population; (ii) further informs how choline improves outcomes in FASD; and (iii) informs the optimization of future choline interventions for at-risk pregnancies and individuals. This study represents an early application of Personalized Medicine to FASD.