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Numerous variables influence the phenotypic outcomes of embryonic Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>exposure. Among these variables, genetics appears to play an important role, yet our understanding of the genetic predisposition to<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>is still in its infancy. We review the current literature that relates to the genetics of<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>susceptibility and gene\u2013Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>interactions. Where possible, we comment on potential mechanisms of reported gene\u2013Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>interactions. Early indications of genetic sensitivity to<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>came from human and animal studies using twins or inbred strains, respectively. These analyses prompted searches for susceptibility loci involved in Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>metabolism and analyses of candidate loci, based on phenotypes observed in<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>. More recently, genetic screens in animal models have provided an additional insight into the genetics of<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>. Understanding<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>requires that we understand the many factors influencing phenotypic outcome following embryonic Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>exposure. We are gaining ground on understanding some of the genetics behind<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>, yet much work remains to be carried out. 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