The coexisting andrological abnormalities (eg, low inhibin B/high FSH, oligoasthenoteratozoospermia, varicocele, small testicular volume) can explain gonadotropin and semen findings but do not account for the near-absence of SHBG caused by SHBG variants in this patient as circulating SHBG is from hepatic origin [3, 13]. This evidence concerns the gene BRD2 and oligoasthenoteratozoospermia.