Teriparatide (human PTH:1-34) is an anabolic therapeutic for the treatment of osteo-porosis. Studies demonstrate variable response to PTH, with up to 44% of patients showing no change in hip bone mineral density (BMD) after 24 months of treatment. We previously showed that the bone response to intermittent PTH varies by strain in mice, suggesting that the response is genetic. In this study, we conducted a genome-wide association mapping study (GWAS) using mice from the Diversity Outbred population (DO). The DO was de-rived by breeding 8 inbred strains of mice together, resulting in individual mice carrying a random assortment of alleles from each of the founder strains. We treated 782 mice with either intermittent PTH (40 μg/kg/day) or saline for 4 weeks, starting at 12 weeks of age (fe-males = 195 PTH, 184 saline, males = 206 PTH, 197 saline). Mice were genotyped using the Giga Mouse Universal Genotyping Array. Trabecular bone volume fraction (BV/TV) was measured in the distal femur by microCT and femur diaphyseal strength was measured via 3-point bending. Genetic loci were mapped by fitting a mixed-effects linear model at each genetic marker and regressing each bone phenotype on the haplotype probabilities. In model 1 PTH treatment was used as an additive covariate, and in model 2 PTH treatment was con-sidered as both an additive covariate and interactive covariate with genotype. We subtracted the peak logarithm of the odds (LOD) for each locus from model 2 from the peak LOD for model 1 to detect genomic loci that interacted with the PTH treatments, as has been previ-ously suggested for estimating sex-specific loci. For model 2 we detected 5 loci for strength that exceeded the LOD threshold of 8 and were shared with model 1, and 4 such loci for BV/TV (Table 1). By subtraction of the LODs, we identified 2 peaks for BV/TV and 1 peak for strength that were suggestive of interacting with PTH treatment to modify the phenotype of interest (Table 1). The largest LOD difference was for the Chr 12 locus for BV/TV. The 1.5 LOD-drop confidence interval for this locus contains 37 protein-coding genes, including Alkbh1, a histone dehydrogenase. Loss of Alkbh1 in mice results in bone ossification de-fects, and among the DO founder strains both missense and splice mutations have been noted that could impact gene function. The results of this study demonstrate that genetic mapping studies in mice have the potential to provide additional insight on how PTH acts on bone.