In a mouse model, cytosolic GPX4 was essential for embryonic development and spermatogenesis [53], and the deletion of mitochondrial GPX4 (mGPX4) also caused male infertility, which in turn led to impaired sperm quality and severe structural abnormalities, reduced sperm motility, and mitochondrial membrane potential [52, 88]. Here, GPX4 is linked to male infertility.