Given that general inhibitors of arginase cause deleterious hyperammonemia due to inhibition of hepatic Arg‐I and that no specific inhibitors of extrahepatic Arg‐II are available, our study could open a new therapeutic avenue for developing specific medications targeting Arg‐II for treatment of chronic inflammatory diseases, including type II diabetes mellitus and atherosclerosis. The gene discussed is LNCARGI; the disease is Hyperammonemia.