Based on limited published evidence, CFAP97D1 is required for male fertility through axonemal doublet stabilization essential for sperm motility. The protein is exclusively expressed in testes and functions in sperm flagellum ultrastructure maintenance 1. CFAP97D1 deletion causes asthenozoospermia and male subfertility, with affected sperm displaying abnormal motility and selective loss of the fourth axonemal doublet 1. The gene is evolutionarily conserved across mammalian and other species, including Chlamydomonas.