In males with hypogonadism, clinical symptoms and the requirement for therapy vary with age. Early fetal-onset hypogonadism causes disorders of sex development (DSD), which manifest as underutilized genitalia, whereas hypogonadism that develops later in fetal life manifests as micropenis, cryptorchidism, and/or micro-orchids. After the time of prenatal stimulation of the gonadal axis has passed, diagnosing hypogonadism is difficult since androgen insufficiency does not become obvious until adolescence. Then, distinguishing between constitutional puberty delay and central hypogonadism might be challenging. Micropenis and/or cryptorchidism are the most common reasons for seeking therapy in infancy and childhood, whereas lack of pubertal development and relatively low height are the most common complaints in adolescence. In the great majority of instances, testosterone treatment has been the standard, although off-label. Alternative therapy, however, has lately been tested: aromatase inhibitors to activate the hypothalamic-pituitary-testicular axis in males with congenital puberty delay and replacement with GnRH or gonadotrophins in individuals with central hypogonadism. Furthermore, priming with follicle-stimulating hormone (FSH) prior to hCG or luteinizing hormone (LH) therapy appeared to be efficient in inducing increased testicular enlargement. Although the justification for gonadotrophin or GnRH therapy is based on emulating normal physiology, long-term findings were required to determine their influence on adult fertility.