A previous polymorphism survey of the type 2 diabetes gene CAPN10 identified a segment showing an excess of polymorphism levels in all population samples, coinciding with localized breakdown of linkage disequilibrium (LD) in a sample of Hausa from Cameroon, but not in non-African samples. This raised the possibility that a recombination hotspot is present in all populations and we had insufficient power to detect it in the non-African data. To test this possibility, we estimated the crossover rate by sperm typing in five non-African men; these estimates were consistent with the LD decay in the non-African, but not in the Hausa data. Moreover, resequencing the orthologous region in a sample of Western chimpanzees did not show either an excess of polymorphism level or rapid LD decay, suggesting that the processes underlying the patterns observed in humans operated only on the human lineage. These results suggest that a hotspot of recombination has recently arisen in humans and has reached higher frequency in the Hausa than in non-Africans, or that there is no elevation in crossover rate in any human population, and the observed variation results from long-standing balancing selection. L INKAGE disequilibrium (LD), the nonrandom association of linked alleles, has attracted great attention in human genetics because of the hope that LD-based association studies may help dissect the genetic basis of common diseases (Risch and Merikangas 1996). Local LD patterns are influenced by a broad range of different factors, which include variation in recombination and mutation rate, natural selection, and demography (Pritchard and Przeworski 2001). Indeed, fine-scale variation in LD decay with distance between sites is well documented in the human genome, and this variation was shown to exceed what is expected if mutation and recombination occurred at a uniform rate and all variation were evolutionarily neutral (Crawford et al. 2004;McVean et al. 2004;Altshuler et al. 2005;Myers et al. 2005). Moreover, recent analyses of LD using population-genetic approaches have suggested that there is extensive heterogeneity in recombination rates over the scale of kilobases (Crawford et al. 2004;McVean et al. 2004;Altshuler et al. 2005;Myers et al. 2005).The notion that variation in LD decay is due largely to variation in recombination rates was bolstered by the analysis of recombinants in sperm samples (Hubert et al. 1994;Arnheim et al. 2003). Sperm-typing studies have demonstrated that crossover events cluster in narrow intervals of 1-2 kb corresponding to regions of localized breakdown of LD (Han et al. 2000;Jeffreys et al. 2001). Moreover, they showed that substantial interindividual variability in recombination rate exists, raising the possibility that hotspots may be short-lived features of the human genome (Yu et al. 1996;Jeffreys and Neumann 2002). Recent cross-species comparisons of LD patterns have further shown that there is little overlap between inferred hotspots in humans and closely related nonhuman primates (Wall et...