In the NO precursor, ARG was effective in minimizing the deleterious alterations associated with HE via reducing hyperammonemia and potentiating the antioxidant response via inhibition of oxidative stress and thus induce Nrf-2, and inhibit NF-κB-mediated apoptosis and thus inhibited its neurological complications. This evidence concerns the gene NFKB1 and hereditary elliptocytosis.