Mendelian transmission is established during meiosis, the cell division that generates haploid gametes (e.g., sperm and eggs) from diploid germ cells. Meiosis does not, however, have to be fair. Selfish genetic elements, or meiotic drivers, have evolved to cheat this process in order to be packaged into functional gametes more often than the expected 50% probability. By biasing allele transmission in their favor, meiotic drive alleles can short-circuit natural selection, causing their spread even if they are harmful to organismal fitness. Indeed, meiotic drive alleles are thought to be directly or indirectly associated with infertility in diverse eukaryotes, from fungi to flies to humans [2]. Drive occurring in male meiosis may have immediate consequences to fertility, potentially facilitating its detection. In contrast, drive in female meiosis could lead to very subtle skews in inheritance patterns and no overt signs of infertility; such driver alleles may therefore go unnoticed even if they are more pervasive [3, 4]. Surprisingly few meiotic drivers have been conclusively identified. There are three major roadblocks to the efficient identification and validation of meiotic drive alleles. First is the prevalent usage of isogenic, lab-domesticated organisms in genetics research; driver alleles can only be identified in heterozygotes. Second, the rapid evolution of suppressors to alleviate the deleterious effects of meiotic drivers can obscure drive in intraspecific crosses and also rapidly extinguish meiotic drive alleles by eliminating their evolutionary advantage [5]. Third, it can often be difficult to distinguish the actions of meiotic drive alleles from inherent viability defects associated with the underrepresented allele. Overcoming many of these limitations, a new report in this issue of PLOS Genetics by de Villena and colleagues provides compelling evidence for a massive copy number expansion that is causally linked to female meiotic drive in mice [6]. Didion et al. began their study by investigating the genetic basis of transmission ratio distortion (TRD) of a region of mouse chromosome 2. This TRD had been previously observed in a number of crosses, including, most recently, in the recombinant inbred Collaborative Cross (CC) lines designed for genetic analyses [7]. TRD was observed in favor of the WSB/EiJ allele across a ~50 Mb region in the middle of chromosome 2 (WSB/EiJ was one of the eight original inbred strains used to create recombinant inbred lines [5]). In the present report, Didion et al.