Homozygous Gpx4 knock-in mice obtained by mutation of Sec into Ala are not viable, but studies on heterozygous animals Gpx4+/− have confirmed that GPx4 deficiency is associated with spermatozoid structural abnormalities and reduced motility, and that the resulting infertility of males is markedly counteracted by concomitant knock-out of the Alox15 gene which codes for 15-lipoxygenase [156]. The gene discussed is GPX4; the disease is Infertility.