In this regard, Zydan et al., in an animal model of the relapsing-remitting experimental autoimmune encephalomyelitis, showed that ALC as a supplementary treatment to dexamethasone results in a significant reduction in MDA and caspase-3 activity and a significant elevation in Bcl-2 and GSH expression and consequently provides considerable antiapoptotic and antioxidant milieu in the spinal cord and brain milieu [47]. The gene discussed is CASP3; the disease is experimental autoimmune encephalomyelitis.