An enduring challenge in the field of population genetics has been to explain how additive genetic variance is maintained in the face of persistent directional selection. Various solutions have been proposed among which prominent examples include environmental fluctuation, mutation-selection balance, frequency-dependent selection, antagonistic selection, and overdominance of heterozygotes. This problem is exacerbated in the case of sexually selected traits, where there is abundant evidence from natural populations that strong, persistent directional selection is relatively common – culminating in the so-called ‘lek paradox’. Thus sex traits may act as good model for a general understanding of how genetic variability is maintained given that they (1) show high intra- and interspecific polymorphism at the genetic and morphological levels despite (2) showing rapid evolution often with strong signatures of directional selection. Our lab has approached the study of sex and reproduction-related traits from a variety of angles. Through early work using two-dimensional SDS-PAGE, it was discovered that proteins expressed in reproductive organs exhibited high divergence between closely related species. These results are supported by more recent work using genomics, developmental, and microarray approaches, which have shown: (1) rapid evolution and higher levels of coding sequence variation in sex-and reproduction-related genes as compared to non-sex genes, (2) faster evolution of male-biased genes as compared to female-biased genes, (3) faster divergence of gene expression in testis and sperm genes, (4) faster evolution of male sex genes during later stages of development, (5) a faster rate of gene orthology loss in male sex genes as compared to female- or non-sex genes, and (6) a higher incidence of new genes and gene-transpositions in male sex as compared to non-sex genes. High within-population variation coupled to high divergence between populations presents a paradox that contradicts the expected loss of genetic variation due to strong sexual selection. In addition to previous solutions (e.g., condition dependence), this paradox can also be resolved by assuming that sexual traits under strong and persistent directional selection will act as a trap for capturing new loci (e.g., retrotransposed/duplicated/denovo genes, amino acid repeats, copy number variation) affecting the trait and thus generate new additive genetic variation. We have previously named this theory as “Male Sex Drive”(Singh and Kulathinal 2005) in the context of sexual traits, however, the framework is general enough to be extrapolated to any trait experiencing strong and persistent directional selection. In addition to explaining the maintenance of genetic variation, this theory also opens a window on the origin of complex quantitative traits, which may arise via the capture of novel genes, and makes the genome open to mutational input in response to directional selection.