Despite strong functional effects of variants in humans, the minor allele frequencies are often too low to attain sufficient sample size. Murine populations such as the BXDs, the Collaborative Cross and heterogeneous stock typically have linkage disequilibrium that is at least an order of magnitude larger than in humans. Consequently, the assignment of specific causality may be erroneous. For example, in the BXD family ∼20,000 protein coding genes and 12,000 coding variants are distributed across ∼4,000 haplotype blocks. Increasing the size and genetic diversity of a reference population and the number of recombination events can improve genetic resolution, but a more effective and meaningful solution, exemplified in this study, is to exploit other mouse cohorts and human cohorts for validation and cross-species translation. For example, by having multiple phenomes for a single species, along with matched databases of segregating sequence variants, it would become practical to rapidly test the replicability of genome–phenome relations. It may soon be practical to compare the BXD phenome with that of the Collaborative Cross and other large families of RI strains. Any cohort will only
