DED patients, as well as those who suffer from Sjogren’s syndrome have also been found to have an increased production and activation of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor-necrosis factor-α (TNF-α), and transforming-growth factor-β (TGF-β), indicating the significant therapeutic implications of treatment with ALA [40]. The gene discussed is IL6; the disease is Sjogren syndrome.