However, little is known about whether the deficiency of α-DIPA in MS-affected patients directly enhance TNF-α and IL-17 signaling and microglia proinflammatory reactions in the CNS, therefore, validation study is needed to be carried out to demonstrate that decreased plasma level of endogenous α-DIPA indeed facilitates inflammation in peripheral system and even in the CNS. This evidence concerns the gene TNF and myeloid sarcoma.