In a later experiment (in 2014), the same group showed that VCE-003 ameliorated the neurological defects and the severity of MOG-induced EAE (myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis) in mice through CB2 and PPARγ receptor activation, at least partially, as antagonists of both these receptors partially blocked VCE-003 activity [35]. This evidence concerns the gene MOG and experimental autoimmune encephalomyelitis.