Predation often has consistent effects on prey behavior and morphology, but whether the physiological mechanisms underlying these effects show similarly consistent patterns across different populations remains an open question. In vertebrates, predation risk activates the hypothalamic-pituitaryadrenal (HPA) axis, and there is growing evidence that activation of the maternal HPA axis can have intergenerational consequences via, for example, maternally-derived steroids in eggs. Here, we investigated how predation risk affects a suite of maternally-derived steroids in threespine stickleback eggs across nine Alaskan lakes that vary in whether predatory trout are absent, native, or have been stocked within the last 25 years. Using liquid chromatography coupled with mass spectroscopy (LC-MS/ MS), we detected 20 steroids within unfertilized eggs. Factor analysis suggests that steroids covary within and across steroid classes (i.e. glucocorticoids, progestogens, sex steroids), emphasizing the modularity and interconnectedness of the endocrine response. Surprisingly, egg steroid profiles were not significantly associated with predator regime, although they were more variable when predators were absent compared to when predators were present, with either native or stocked trout. Despite being the most abundant steroid, cortisol was not consistently associated with predation regime. Thus, while predators can affect steroids in adults, including mothers, the link between maternal stress and embryonic development is more complex than a simple one-to-one relationship between the population-level predation risk experienced by mothers and the steroids mothers transfer to their eggs. Predation is a potent force that shapes phenotypes over evolutionary and developmental time 1,2. A major question in evolutionary biology is the extent to which selective pressures such as predation pressure have predictable effects on prey phenotypes and the role of natural selection in shaping consistent patterns of plasticity and/or the independent evolution of similar traits in closely related lineages (i.e. parallelism 3-6). Examining whether different populations of prey respond to predators in the same manner has offered insights into this question 7. For example, traits that protect prey and/or enable quick escape from predators often show evidence of parallelism across replicate populations with similar predation regimes (e.g. morphology 7,8 ; antipredator behavior 9,10). Predation pressure has also been shown to affect life history traits (e.g. age and size at maturity, offspring size and number), often in a parallel manner across populations with similar predation regimes 11,12. Despite the many studies comparing morphology, behavior, and life history traits among populations that differ in predation risk, less is known about the predictability of changes in physiological mechanisms underlying these phenotypic responses to predation pressure. The physiological response to acute and chronic stressors such as predation risk is highly conserv...