Some studies implicate that targeting Arg-I is also beneficial for cardiovascular functions, these studies are solely dependent on the pharmacological inhibitors, which inhibit both isoforms of arginases (97–99), since systemic Arg-I deficient mouse exhibits severe symptoms of hyperammonemia, and die between postnatal days 10 and 14 (31), one should consider that these inhibitors could inhibit liver Arg-I, resulting in hyperammonemia. The gene discussed is LNCARGI; the disease is Hyperammonemia.