Indeed, nearly all pathogenic gene variants that have been described to contribute to asthenozoospermia and male infertility in humans (CASTSPER, SLC26A3, SLC26A8, SLC9C1, VDAC, SLO3) were supported by studies using KO mouse models that show a similar phenotype and pathology. This evidence concerns the gene SLC26A3 and Reduced sperm motility.