Along with imbalances in NLR, an altered Th17/Treg ratio also contributes to the upregulation of the above-mentioned proinflammatory (e.g., IL-6, TNFα) and profibrotic (e.g., TGF-β) cytokines, which in turn leads to a hyperactivation of the IL-17 axis, implicated in the progression of NAFL to NASH [66]. This evidence concerns the gene IL6 and non-alcoholic fatty liver.