NOA affects approximately 60% of azoospermic males and includes non-obstructive causes of azoospermia, such as toxic exposures or abnormal testicular development.8 NOA results from either primary testicular failure (elevated LH, FSH, small testes affecting up to 10% of men presenting with infertility), secondary testicular failure (congenital hypgonadotropic hypogonadism with decreased LH and FSH, small testes), or incomplete or ambiguous testicular failure (either increased FSH and normal volume testes, normal FSH and small testes, or normal FSH and normal testis volume).6 This evidence concerns the gene BRD2 and Infertility.