The potential impact of prenatal alcohol exposure (PAE) varies considerably among exposed individuals, with some displaying serious alcohol-related effects and others showing few or even no overt signs of a fetal alcohol spectrum disorder (FASD). In animal models variables such as nutrition, genetic background, health, other drugs, and stress, as well as dosage, duration and gestational timing of alcohol exposure can all be controlled in a way not possible in a clinical situation. In this review we examine mouse PAE models and focus on those with demonstrated craniofacial malformations, abnormal brain development, or behavioural phenotypes that may be considered FASD-like outcomes. Analysis of these data should provide a valuable tool for researchers wishing to choose the PAE model best-suited to their research questions or to investigate established PAE models for FASD comorbidities. It should also allow recognition of patterns linking gestational timing, dosage and duration of PAE with FASD-like outcomes. The latter could be particularly insightful and lead to a better understanding of the molecular mechanisms underlying FASD.