The accumulation of this inflammatory hepatic Th17 (ihTh17) subset was regulated through a CXCL9/10-CXCR3 axis, and these cells were sufficient to exacerbate NAFLD pathogenesis through glycolysis-facilitated production of proinflammatory cytokines IL-17A, TNF, and IFN-γ (16). This evidence concerns the gene IL17A and metabolic dysfunction-associated steatotic liver disease.