However, in both the species LH is absolutely required for ALc function (83) as evident from various mouse models [hpg (13), LH-RKO (91), LH-βKO (92) and ARKO (93, 94)], etc and mutations in human LH-β/LHCGR genes resulting masculinized fetus but compromised pubertal development and complete azoospermia due to total absence of functional pituitary LH and testicular T (100). The gene discussed is PLOD1; the disease is Azoospermia.