The ideal treatment for these forms of hypogonadism, with predominantly central etiopathogenesis (low serum total testosterone (TT) and normal/low serum gonadotropin levels), should be able to increase testosterone levels without suppressing the hypothalamic-pituitary-testicular axis, while maintaining a safety profile on other parameters, such as prostate-specific antigen (PSA) levels and hematocrit, alterations in which represent the main problem with an excess of hormone replacement therapy. The gene discussed is KLK3; the disease is hypogonadism.